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Prof Trevor Marshall
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Bane found this important article:

"Even Bacteria Get Lonely"

http://news.discovery.com/animals/bacteria-solitary-confinement-infection.html

"But what happens when there are high levels of autoinducers but only one bacterium?

Until now the technology to create glass cages 20 micrometers wide to hold bacteria three to four micrometers long didn't exist. Now nanotechnology has advanced to the point where scientists can trap these tiny organisms in glass cages and watch the imprisoned bacteria, in this case Staphylococcus aureus, talk to themselves.

The conversations are angry. The bacteria know their messages, or quorum sensing molecules, are going nowhere. If the chemicals can't move anywhere then neither can much larger bacteria. If bacteria can't move it means they are trapped, either inside a tissue or inside another cell, usually a macrophage, that is attempting to destroy the invading cell.

Either way, bacteria needs to get out, and they activate genes that will help them escape. The Staph produces lysosomes, chemical bombs that eat away at whatever they touch, and releases them into the environment around it. Since the cage is glass, the lysosomes are ineffective, but the bacteria continue to pound the walls with them.

A bacterial change like this isn't supposed to happen. A quorum of chemicals from dozens, hundreds of bacteria packed close together is supposedly the only way for a bacteria to alter its gene expression.

"This is really a way for cells to fight back, to adapt to any condition a cell finds itself in," said Brinker. "All that's needed is a quorum of one."
 

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So, now I'm curious what implications this has for how we go about killing the bacteria.

Is this typical or atypical (trapping the bacteria) in the process of going after them with either the abx or with just an activated immune system?

And, are there other substances (foods or drugs) that interfere with certain chemicals or block messaging in a way that can affect whether bacteria get trapped or not?

Marysue

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What an interesting finding, it may certainly help explain the immunopathology people experience as the immune system starts to function properly. The bacteria simply don't like being killed and so they've found ways to try to fight back! :shock:

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One can really feel the anger of the little beast in the picture. Well....I'm sorry, but if it's gonna be me or him/her .. I hope it's me that survives

Prof Trevor Marshall
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IMO There are several important things brought out by this magnificent study. Here are the main ones.

First - the bacterial cells are reported to actually produce lysosomes. That is very interesting, as it has been my contention for some time that the intraphagocytic metagenomic microbiota has evaded discovery for so long by hiding in the phagocytic lysosomes, which are normally seen under a microscope, and ignored. Additionally, lysosomes could provide the mechanism whereby the microbiota initially becomes internalized in the phagocytes.

Second, several months ago a paper reported that epinephrine, adrenaline, is a quorum sensing hormone for at least one species, an e-Coli bacterium. One of the missing pieces to the clinical puzzle is why Th1 patients are more sensitive to epi/adrenaline, and therefore more sensitive to stress, than healthy individuals. This paper might have provided us a glimpse of such a mechanism - activation of the microbiota by even normal, healthy, levels of adrenaline. Hmmm... stress exacerbates disease, disease exacerbates stress - that certainly matches what happens in practice :)
 
The pace of advances in basic science is quite amazing at the moment...

..Trevor..
 

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The secret, social lives of bacteria: Exclusive interview with Bonnie Bassler

http://blog.ted.com/2009/04/the_secret_soci.php

I spend half my time thinking, "My God, I can't believe they do this!" and then the other half thinking, "Why did it take me so long to figure this out? Of course they do this!" I agree, it's obvious in retrospect.

I often think, "Why is it that my lab that's doing this?" Bacteria have been intensively studied for 400 years. How could this have been missed for nearly 390 of those years? I guess there was this sort of snobbery -- among bacteriologists and among scientists in general -- that because bacteria seemingly live this mundane primitive life, and they have so few genes, and are so tiny, that we could not imagine they possessed this level of complexity and sophistication.

But think about multicellularity on this Earth. Every living thing originally came from bacteria. So, who do you think made up the rules for how to perform collective behaviors? It had to be the bacteria.

Again, even after we knew about intra-species quorum sensing, when we discovered the cross-species signaling molecule, we were shocked. But in retrospect, of course they have to signal across species! It doesn't do bacteria any good to only count their siblings if there are all kinds of other species around. It all makes total sense, right? But you can't know that until you figure it out. The bottom line is that we are always underestimating them.

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And here a Video with Bonnie Basler about the different "languages" Bacteria use to communicate to each others. May be cytokines are just a further evolutionary development of such communication, allowing coordinated actions.

The Secret, Social Lives of Bacteria

http://www.youtube.com/watch?v=TVfmUfr8VPA

Alex

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Trevor wrote:
First - the bacterial cells are reported to actually produce lysosomes. That is very interesting, as it has been my contention for some time that the intraphagocytic metagenomic microbiota has evaded discovery for so long by hiding in the phagocytic lysosomes, which are normally seen under a microscope, and ignored. Additionally, lysosomes could provide the mechanism whereby the microbiota initially becomes internalized in the phagocytes.
http://en.wikipedia.org/wiki/Lysosome
After reading the definition of lysosome....I'm wondering...
What possible purpose would bacteria benefit from producing lysosomes?
And, if lysosomes are the cells garbage disposal system, how are the bacteria using this as a place to hide inside the phagocytes?
Wouldn't the enzymes inside the lysosome eat up the bacteria?

Marysue

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Marysue, have you identified which enzymes are inside the lysosomes? Have you checked to see whether they indeed function as garbage disposal system?

In truth, there is no way to do this. IMO That is why a flawed concept of "garbage disposal" has persisted for so long. I mean, the Wikipedia old-wives-tale just sounds so sensible, doesn't it?

..Trevor..
 

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Sneaky Little Buggers!:?


http://en.wikipedia.org/wiki/Autophagy_(cellular)


Autophagy, Immunity, and Microbial Adaptations
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2720763/

Autophagy adjusts cellular biomass and function in response to diverse stimuli, including infection. Autophagy plays specific roles in shaping immune system development, fueling host innate and adaptive immune responses, and directly controlling intracellular microbes as a cell-autonomous innate defense. As an evolutionary counterpoint, intracellular pathogens have evolved to block autophagic microbicidal defense and subvert host autophagic responses for their survival or growth. The ability of eukaryotic pathogens to deploy their own autophagic machinery may also contribute to microbial pathogenesis. Thus, a complex interplay between autophagy and microbial adaptations against autophagy governs the net outcome of host-microbe encounters.

"The greatest threat to an intracellular pathogen imposed by autophagy is not the process of autophagic sequestration per se, but rather the danger imposed by delivery to an autolysosome. Accordingly, it is not surprising that several viruses and intracellular bacteria seem to block fusion of the autophagosome or autophagy protein-dependent fusion of another pathogen containing compartment (i.e., phagosome or pathogen-containing vacuole) with the lysosome."


 

The Autophagic Induction in Helicobacter pylori-Infected Macrophage
http://ebm.rsmjournals.com/cgi/content/full/234/2/171

Helicobacter pylori has developed several mechanisms to evade the intracellular killing after phagocytosis. In this study, we reported that some Taiwanese clinical isolated H. pylori can multiply in human monocytic cells, such as THP-1 or U937 cells, but not in murine macrophage Raw264.7 cells. After internalization, there was a 5- to 10-fold increment of re-cultivable H. pylori from the infected THP-1 cells at 12 hrs post infection. The dividing H. pylori was found in a double-layer vesicle, which is characteristic of autophagosome. The formation of autophagosomes is associated with the multiplication of H. pylori in THP-1 cells. Its modulation with rapamycin or 3-MA affects the level of H. pylori replication. Furthermore, the VacA or CagA mutants of H. pylori have lower levels of multiplication in macrophages. We conclude that H. pylori infection induces autophagosome formation, and these autophagic vesicles were adapted for the multiplication of H. pylori in the host.

 

Autophagy in intracellular bacterial infection.
http://www.ncbi.nlm.nih.gov/pubmed/19303905

In this review we have summarized the interaction between autophagy and different bacterial pathogens including those that take advantage of the host cell autophagy, allowing successful colonization, as well as those microorganisms which are controlled by autophagy as part of the innate surveillance mechanism.

 

When Helicobacter pylori invades and replicates in the cells.
http://www.ncbi.nlm.nih.gov/pubmed/19270492

Autophagosome formation is induced by Helicobacter pylori infection and these autophagic vesicles are adopted for replication of H. pylori and subsequent eradication of the invading H. pylori in macrophages. Some Taiwanese clinical isolates of H. pylori can replicate in certain macrophage cell lines. After entry, there was a 5-10 fold increment of recultivable H. pylori from the infected permissible cells at 12 h post infection. The dividing H. pylori are observed to reside in double-layered autophagosomes. Therefore, H. pylori can be considered as a kind of intracellular microorganism. The autophagy induction by H. pylori is not only found in macrophages, but also in dendritic cells and gastric epithelial cells. This new finding has several implications for the life cycle of H. pylori in the host. The bacterium's residence inside infected cells will increase its resistance to antimicrobial treatment, avoid neutralization by anti-H. pylori antibodies, impair antigen presentation, and alter the cellular immune response. The replication of H. pylori in autophagic vesicles, and the consequences of this provide an important hint as to why this microorganism causes such a broad spectrum of diseases.

 

Division of the Salmonella-containing vacuole and depletion of acidic lysosomes in Salmonella-infected host cells are novel strategies of Salmonella enterica to avoid lysosomes.
http://www.ncbi.nlm.nih.gov/pubmed/19858305

Salmonella has evolved several strategies to counteract intracellular microbicidal agents like reactive oxygen and nitrogen species. However, it is not yet clear how Salmonella escapes lysosomal degradation. Some studies have demonstrated that Salmonella can inhibit phagolysosomal fusion, whereas other reports have shown that the Salmonella-containing vacuole (SCV) fuses/interacts with lysosomes. Here, we have addressed this issue from a different perspective by investigating if the infected host cell has a sufficient quantity of lysosomes to target Salmonella. Our results suggest that SCVs divide along with Salmonella, resulting in a single bacterium per SCV. As a consequence, the SCV load per cell increases with the division of Salmonella inside the host cell. This demands more investment from the host cell to counteract Salmonella. Interestingly, we observed that Salmonella infection decreases the number of acidic lysosomes inside the host cell both in vitro and in vivo. These events potentially result in a condition in which an infected cell is left with insufficient acidic lysosomes to target the increasing number of SCVs, which favors the survival and proliferation of Salmonella inside the host cell.




Last edited on Tue Apr 6th, 2010 12:11 by Bane

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Bile Sends Mixed Signals to E. Coli

http://www.sciencedaily.com/releases/2010/03/100330210940.htm

Bile is secreted into the small intestine and exerts an antibacterial effect by disrupting bacterial membranes and damaging bacterial DNA. While bile is a human defence mechanism, Dr Hamner and colleagues from Montana State University and the University of New England found that some bacteria such as Escherichia coli O157:H7 -- an important food-borne pathogen -- have evolved to use the signal to their advantage. These bacteria use the presence of bile as a signal to tell them that they are in the intestine which allows them to adapt and prepare to cause disease.

 

Flu Jab for Bacteria

http://www.sciencedaily.com/releases/2010/03/100331201535.htm

Specific bacterial proteins recognise infectious viruses, called bacteriophages, by detecting foreign DNA. These proteins take the viral DNA and insert it into the bacterial genome at very specific locations. "Storing the information in this way gives the bacteria a lasting 'memory' of the harmful virus that subsequently confers immunity- much like our own immune systems," said Professor van der Oost. Upon future attack by the same virus, the DNA sequence of the invader is quickly recognised and destroyed by the bacteria.



Last edited on Tue Apr 6th, 2010 10:33 by Bane

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Dr Trevor Marshall wrote:
Marysue, have you identified which enzymes are inside the lysosomes? Have you checked to see whether they indeed function as garbage disposal system?

In truth, there is no way to do this. IMO That is why a flawed concept of "garbage disposal" has persisted for so long. I mean, the Wikipedia old-wives-tale just sounds so sensible, doesn't it?

..Trevor..

Thanks Trevor. This really is one of my biggest sources of confusion now with all the reading and learning I've been doing. Some of the basic descriptions about cellular function may be accurate while others are just something that's been stated to fill in the gaps in our learning without any real science behind it. And, clearly, I don't know the difference. ;)

Also, if bacteria are producing lysosomes (assuming that finding is sound), there is most certainly a reason for it and something they have to gain by doing so.

Marysue

Last edited on Tue Apr 6th, 2010 12:19 by Marysue

Prof Trevor Marshall
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Marysue,
All Science is based on 'models'. I have a model of the Th1 disease process in my head. This allows me to understand what is happening, and predict what might happen next.

For example, Relativity is a model. It is still being tested, one century after it was proposed, and half a century after the first atomic bomb. Models don't have to be perfect to be useful, and they don't have to be perfect to persist.

I suspect that the assessment of "lysosomes" in this experiment was based on what they looked like, rather than any direct analysis. However, this observation fits with our model, and so it adds to our model. Wirostko imaged a sub-microscopic transparent globule, probably which would be described as a 'lysosome', emerging from one of the phagocytes under his Electron Microscope -- it all fits into place in my 'model'.

'Vitamin' D is another model...

..trevor..
 

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Bane,

Since learning that NOD2 is (strongly) transcribed by the VDR back in late fall, I've been doing a bit of digging and what I have found is really fascinating.  NOD2 is an intracellular pathogen recognition receptor which recognizes muramyl dipeptide (MDP) found in certain bacteria.  NOD2 has been linked with a number of TH1 diseases including Crohn's, IBD, psoriatic arthritis, Blau syndrome and is also thought to play a critical role in the maintenance of gut flora homeostasis. 

Activation of NOD2 leads to the expression of Human Beta Defensin2.  Interestingly, it may also recognize viral ssRNA leading to activation of the IFN response.  I found one paper that indicated it may work synergistically with TLR3 in amplifying the expression of RNaseL (think xmrv/prostate cancer).

What I have found most interesting is that a number of recent papers have discussed NOD2 as being a potential bridge between innnate immunity and autophagy.  Then again, autophagy may simply be part of the innate immune system rather than a completely separate system. 

Of course, if the transcription of VDR target genes is disrupted then autophagy would also be disrupted via decreased NOD2 expression.  Decreased autophagy may lead to the gradual accumulation of various intracellular proteins which are normally broken down.  Could perturbed autophagy caused by suboptimal NOD2 expression be associated with the accumulation of amyloid beta deposits in alzheimers? 

A recent paper came out indicating that 1,25D and curcumin (a VDR agoinst) both lead to the clearance of amyloid beta deposits.  I wonder if this occurs through NOD2 expression and the induction of autophagy (as well as elimination of the bugs that block the VDR).

http://www.ncbi.nlm.nih.gov/pubmed/20200479

Nod proteins link bacterial sensing and autophagy.

Autophagy is one of the main cellular degradation systems in eukaryotes, responsible for the elimination of long-lived proteins and damaged organelles. Besides its well-documented role as a housekeeping mechanism, autophagy has recently caught the attention of groups working in the fields of microbiology and immunology, especially those working in innate immunity. In particular, the highly specific segregation and degradation of intracellular bacteria by the autophagic machinery was a matter of great interest. However, it was still unclear how the autophagy machinery could target intracellular bacteria with such specificity. We have recently analyzed the role of the intracellular peptidoglycan (PG) receptors Nod1 and Nod2 as a link between intracellular bacterial sensing and the induction of autophagy. Our results demonstrated that Nod2 recruits the critical autophagy protein ATG16L1 to the plasma membrane during bacterial invasion and that cells expressing mutations in these proteins-two of the most important associated with Crohn disease-autophagy is defective upon infection or stimulation with the bacterial peptidoglycan fragment MDP. Thus, our findings put together two genes previously reported as independent risk factors for the development of Crohn disease and open a venue in the study of new therapies to cure the disease.

 

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Interesting thinking Philly!:) So if the VDR isn't working or present, that could mean less or missing NOD2??;)



Direct and indirect induction by 1,25-dihydroxyvitamin D3 of the NOD2/CARD15-defensin beta2 innate immune pathway defective in Crohn disease.

http://www.ncbi.nlm.nih.gov/pubmed/19948723

Here we show that hormonal vitamin D, 1,25-dihydroxyvitamin D(3), robustly stimulates expression of pattern recognition receptor NOD2/CARD15/IBD1 gene and protein in primary human monocytic and epithelial cells.

 

Activation of innate host defense mechanisms by Borrelia.

http://www.ncbi.nlm.nih.gov/pubmed/20146985

Toll-like receptors (TLRs), NOD-like receptors (NLRs) and C-type lectin receptors (CLRs). TLR2 has been found to be the most important receptor of the TLRs. The intracellular receptor NOD2, a member of the NLRs, might also play an important role in recognition.

 

Differential roles for NOD2 in osteoblast inflammatory immune responses to bacterial pathogens of bone tissue.

http://www.ncbi.nlm.nih.gov/pubmed/20360399

Osteoblasts produce an array of immune molecules following bacterial challenge that can contribute to inflammation and the recruitment of leukocytes to sites of infection during bone diseases such as osteomyelitis. However, the mechanisms by which osteoblasts perceive and respond to facultative intracellular pathogens such as Salmonella species and Staphylococcus aureus have not been determined. Recently, our laboratory has described the expression in osteoblasts of members of the nucleotide-binding domain leucine-rich repeat region containing family of proteins that include nucleotide-binding oligomerization domain-2 (NOD2), a molecule that functions as an intracellular receptor for bacterial peptidoglycans. In the present study, we demonstrate that NOD2 expression is required for select inflammatory mediator production by osteoblasts following infection with the invasive pathogen, Salmonella. In contrast, we have found that the inflammatory immune responses of osteoblasts to the passively internalized bacterial species, S. aureus, heat killed pathogenic Salmonella, a non-invasive Salmonella strain, and specific Toll-like receptor ligands, are not reduced in the absence of NOD2 expression but are, in fact, elevated. Based upon these findings, we suggest that NOD2 serves differential roles in osteoblasts, promoting inflammatory responses to invasive bacteria while tempering cell responses to extracellular and/or passively internalized bacterial species.

Last edited on Wed Apr 7th, 2010 13:11 by Bane

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Dr Trevor Marshall wrote: IMO There are several important things brought out by this magnificent study. Here are the main ones.

Second, several months ago a paper reported that epinephrine, adrenaline, is a quorum sensing hormone for at least one species, an e-Coli bacterium. One of the missing pieces to the clinical puzzle is why Th1 patients are more sensitive to epi/adrenaline, and therefore more sensitive to stress, than healthy individuals. This paper might have provided us a glimpse of such a mechanism - activation of the microbiota by even normal, healthy, levels of adrenaline. Hmmm... stress exacerbates disease, disease exacerbates stress - that certainly matches what happens in practice :)
 
The pace of advances in basic science is quite amazing at the moment...

..Trevor..
 

here is that paper: 

Gene  

http://jb.asm.org/cgi/content/full/186/8/2281 

“the mammalian hormone epinephrine can substitute for autoinducer in the QS system of enterohemorrhagic Escherichia coli.  Thus, autoinducers and hormones may be interchangeable in a language common to prokaryotes and eukaryotes”

Last edited on Thu Apr 8th, 2010 17:56 by edj2001

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Thx, Ed - an interesting find, but I think this is the one Trevor might have referred to  (quoted under reference 23) ?? - but it's fairly old ??

http://www.pnas.org/content/100/15/8951.abstract?ijkey=80547fd4abd4ed47a85e84a19262e161beefc714&keytype2=tf_ipsecsha

(click "full text" in the box to the right of the abstract).

Here is another one:
http://www.biomedcentral.com/1471-2164/9/458

note this:
"However, adrenaline may also serve in favour of the host defences by lowering antimicrobial peptide resistance and hence documenting for the first time such a function for a hormone."

Btw, see also this thread from December 09:
http://www.marshallprotocol.com/view_topic.php?id=13545&forum_id=11

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Gene linked to the paper which was in my mind, but the links given by Ron are also fascinating. Thanks to you both :)
 

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(from Phillip Tierno, PhD, director of clinical microbiology and diagnostic immunology at the New York University Langone Medical Center and author of The Secret Life of Germs)
on 6 habits that make you sick, in
http://www.webmd.com/allergies/living-with-allergies-10/6-daily-habits-that-may-make-you-sick?page=3
on the 5th habit webMD has a delightful misprint:
refers to "a bedroom where bacteria are teaming"
QS to be sure, to be sure :P

Bane
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Dr Trevor Marshall wrote:
Second, several months ago a paper reported that epinephrine, adrenaline, is a quorum sensing hormone for at least one species, an e-Coli bacterium. One of the missing pieces to the clinical puzzle is why Th1 patients are more sensitive to epi/adrenaline, and therefore more sensitive to stress, than healthy individuals. This paper might have provided us a glimpse of such a mechanism - activation of the microbiota by even normal, healthy, levels of adrenaline. Hmmm... stress exacerbates disease, disease exacerbates stress - that certainly matches what happens in practice :)
 
The pace of advances in basic science is quite amazing at the moment...

..Trevor..
 



PANDAS don't like stress

http://www.physorg.com/news190034694.html

http://en.wikipedia.org/wiki/PANDAS

http://www.journals.elsevierhealth.com/periodicals/bps/article/S0006-3223(09)01019-1/abstract

"In a new longitudinal study appearing in Biological Psychiatry, published by Elsevier, researchers identified new infections in children and adolescents with Tourette syndrome (TS) and/or OCD, and compared them with healthy control subjects. They also measured the participants' levels of emotional stress. Prior research has shown that stress is an important factor in developing depression, and that individuals with TS or OCD tend to be particularly sensitive to stress.

They then used this data to examine the power of the infections and measures of psychosocial stress to predict future tic, obsessive-compulsive, and depressive symptom severity.

Dr. James Leckman, senior author of this project, explains their findings: "We found that periods of tic and OC symptom worsening were independently associated with antecedent newly diagnosed strep infections as well as higher levels of antecedent psychosocial stress. When we looked at just the PANDAS, we also found similar results."

In other words, stress may aggravate the impact of prior streptococcal infection in promoting symptoms of TS and OCD. There was no impact of prior streptococcal infections on depressive symptoms."

 

Sneeze girl gets a diagnosis

http://today.msnbc.msn.com/id/26184891/vp/34325311#34325311

 

 



Last edited on Sat Apr 10th, 2010 18:59 by Bane

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This is a very interesting thread. Epinephrine/adrenaline is a big problem for me.

I have found the research of Manuel Martinez-Lavin MD, Rheumatologist provides a very reasonable theory of the cause of the symptoms in people with FM (and probably many other Th1 diseases).

http://www.martinez-lavin.com/Fibromyalgia.htm 
 
"What is heart rate variability analysis?

Heart rate variability analysis is based on the fact that the heart rate is not constant, but varies continuously by a few milliseconds. The periodic components of this heart rate variation are dictated by the input of the two branches of the autonomic nervous system: the sympathetic nervous system and the parasympathetic nervous systems. These two branches have antagonistic effects on most bodily functions. Time and frequency domain analyses are able to estimate the relative effect of each branch on the periodic variations of the heart rate. The elegance of this new method resides in the fact that all measurements are derived from electrocardiograms, so patients are not subjected to any discomfort.

 
Our research on fibromyalgia.

We studied a group of patients with fibromyalgia and compared them with healthy controls. By means of portable recorders, we registered the subjects' heartbeat for 24 hours while they followed their routine daily activities. We found that patients with fibromyalgia have relentless hyperactivity of the sympathetic nervous system. This abnormality was also evident during sleeping hours. In a different study, we subjected patients with fibromyalgia to a simple stress test (to stand up). We observed a paradoxical derangement of the sympathetic nervous system response to the upright posture. Such findings have been confirmed by other groups of investigators.

The results of these studies suggest that a fundamental alteration of fibromyalgia is a disordered function of the autonomic nervous system. Patients with fibromyalgia lose the normal day/night cycles (circadian rhythms) and have a relentless sympathetic hyperactivity throughout 24 hours. This may explain the sleeping problems that the patients have. At the same time, such individuals have sympathetic hypo-reactivity to stress, which could explain the profound fatigue, morning stiffness and other complaints associated to low blood pressure. This autonomic nervous system dysfunction could induce other symptoms of fibromyalgia such as irritable bowel, urinary discomfort, limb numbness, anxiety and dryness of the eyes and mouth."

 
 

Is it possible that the "relentless sympathetic hyperactivity" and "sympathetic hypo-reactivity to stress" are due to the 1,25 D docking into other nuclear receptors and messing with the normal balance and function of other hormones including adrenaline?

Last edited on Sun Apr 11th, 2010 14:56 by Rosie

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2772072/
 
Fut Rheumatol. 2008 October 1; 3(5): 475–483
 
Heart rate variability as a biomarker of fibromyalgia syndrome
Roland Staud, MD
 
Conclusion
 
Autonomic dysfunction of FM patients seems to be strongly associated with reduced total power of HRV, low vagal tone, decreased baroreceptor sensitivity and increased sympathetic activity [60,68]. Such ANS abnormalities have not only been associated with greater risk of developing hypertension [69], but also greater mortality, mostly from cardiovascular causes [70]. Interestingly, several epidemiological studies have reported significantly increased mortality of FM patients compared with matched controls [71,72], but the decreased long-term survival of FM patients was not associated with cardiovascular diseases but with malignancies and infections. ANS dysfunction may have contributed to this poor outcome. Future studies will be necessary to assess whether ANS abnormalities play an important role in the increased mortality of FM patients.

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This information makes me think of two things.  One, the cardiac symptoms are obviously due to the bacteria involvement and it's defestating effects on the heart tissue.  Two, the autonomic nervous system involvement explains why we who suffer from FM have frequent palpitations.  The palpitations become more obvious and occur more often with the MP.  I use to think it was a side effect of Benicar, but as I progress on the protocol one realizes that it is the MP doing it's job of uncovering these nasty bugs.:shock:

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:)

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Rosie,

I also believe that latent intracellular bacteria are affecting so many of us, specifically in the nervous system (nerves of various systems).

With their reproduction cycles, and or our immune functions waxing and waning, these bugs can cause the intermittent "flutters" so many of us experience(d).

I personally believe that the nerve involvement triggers a host of ailments down the line, and this is also one very large reason it is hard to track down for the medical community.

One cause, many different symptoms I've been thinking.

:D

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Stress may be a trigger of bowel disease symptoms

http://www.reuters.com/article/idUSTRE63F3AW20100416

"This is among the first evidence to show that the perception of stress had a direct association with disease course," Dr. Charles N. Bernstein, the lead researcher on the new study, told Reuters Health in an email.

BIGDOG
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Hmmm,

Stress = adrenaline dump = trigger for certain Th1 critters

I also wonder if isn't a nasty little cycle.

Some of these successful bugs share certain genes...

I've noticed so many individuals become very very upset and erratic with a sudden trigger of fear, startling, scare, or sudden excitement.

I would just observe and wonder why such a "small" trigger would induce such a seemingly disproportionate response, often in anger, rage, or physically rash movements... most notable not rational.

I am now thinking that the adrenaline and/or it's analougs are triggering latent critters into releasing some compounds, which profoundly affect us.

Or, a chain of events...

It just fits so well.

I hope Dr. M. and Co. can elucidate some of the macro steps.

:)

Aunt Diana
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I can truly relate to your idea....I have never been as calm as I am now after 3 years of the MP. I used to get hysterical over things that today would probably bother me, but I would be able to think them through.

Knochen
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I have never been as calm as I am now after 3 years of the MP
I can say the same thing, except when the herxing comes back and hits me.  Then I am as edgy as I ever was and tend to be very verbal and excitable.  Had a bad day at work where that came up and bit me not long ago.  The fight's not over yet, but I can see what part the bugs play in the emotional aspects.  Since neural repair is the last to happen, I'm hoping that the neural herxing is a sign that I'm in the final push. 


Bane
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U-M study sheds light on the biological roots of post-traumatic stress disorder

http://www.ns.umich.edu/htdocs/releases/story.php?id=7673

The researchers identified numerous genes—most of them involved in regulating the immune system—that appeared to be more active in people with PTSD. Previous studies have posited a link between altered immune function and PTSD. The new U-M findings support that model and go a step further by identifying a specific biochemical reaction that may be involved.

eClaire
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Hmmm... seems to me I remember Dr. Marshall saying that PTSD was immune related! :D:D:D

Great find!  Thanks a lot!!!

Forwarding to my psychologist....

Claire

Phillyguy
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http://www.ncbi.nlm.nih.gov/pubmed/20441518

Recognition of Borrelia burgdorferi by NOD2 is central for the induction of an inflammatory reaction.

Toll-like receptor 2 (TLR2) plays an important role in the recognition of Borrelia bacteria, the causative agent of Lyme disease, but the existence and importance of additional receptors in this process has been hypothesized. In the present study, we confirmed the role played by TLR2 in the recognition of Borrelia bacteria but also demonstrated a crucial role for the intracellular peptidoglycan receptor NOD2 for sensing the spirochete. Cells from individuals who were homozygous for the loss-of-function mutation 3020insC in the NOD2 gene were defective with respect to cytokine release after stimulation with Borrelia species, and this was confirmed in peritoneal macrophages from mice lacking RICK, the adaptor molecule used by NOD2. In contrast, NOD1 played no major role in the recognition of Borrelia spirochetes. This raises the intriguing possibility that recognition of Borrelia spirochetes is exerted by TLR2 in combination with NOD2 and that both receptors are necessary for an effective induction of cytokines by Borrelia species. The interplay between TLR2 and NOD2 might not only be necessary for the induction of a proper immune response but may also contribute to inflammatory-induced pathology

titta
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Bacteria do not only get lonely.....but criminal, too......and organized ....

The quintessence is already known but it is enjoyable

Mafia Wars


http://www.the-scientist.com/2010/6/1/40/1/


Titta

PGA Terry
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The lack of these key cell membrane components, however, is not without consequences, Rikihisa adds. Without LPS and peptidoglycan, “their membrane structure becomes more fragile,” she says. To compensate, the bacteria take up cholesterol from host cells, which stabilizes their membranes. In fact, Rikihisa and her colleagues found that A. phagocytophilum infection rates were 10 times higher in mice fed a high-cholesterol diet than in those on a normal diet.2 “So the cholesterol is helping [the pathogen],” she says.

Read more: Mafia Wars - The Scientist - Magazine of the Life Sciences http://www.the-scientist.com/2010/6/1/40/1/#ixzz0rH9rlII2
 

 
My cholesterol levels have been consistently low, 140-160mg/dl during the last 20 years that I've been ill. I wonder if this explains my chronically low cholesterol readings. The lower my cholesterol the less I have weighed and the worse I felt. I am now 135 lbs., 30 lbs. under my weight when I was young and healthy. My lowest weight was 115 lbs., 50lbs underweight and at my lowest cholesterol readings, before I started the MP.

Terry 

                                                

minski2
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"Sneeze girl gets a diagnosis"

.............the junk they dish out to us is mind-boggling!!!!!


My 65 year old Uncle sneezed for 3 weeks in the 1950's........PANDA...Pleease!!!!!!!

Dian
 

eClaire
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Terry, my overall cholesterol has been high, approaching 300, though the balance is good, and I have been very sick.  Many folk with ME/CFS have high cholesterol.  I never bought the link between cholesterol and heart disease, and sure enough the talk is almost all about inflammation now even though cholesterol medication is given out like candy.  That was the only drug I would not try to the great frustration of my doctor. 

It seems to me that the various pathogens that makes up a single person's microbiota might have different uses for different things and therefore promote whatever ecology it needs.

My two cents... Claire

PGA Terry
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I think you're right on, Claire. My mix of microbiota is probably quite different than yours, plus our differences in genetic makeup. Since starting the MP I've gained 15 lbs  :) and I wonder if my cholesterol has increased as well.

Terry

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   I want to express some musing on our immune system during 3 years of productive malaise 'fighting off infections' on the MP.
   We have a plethora of examples of clever parasites manipulating the immune system to their advantage, often to placate or blindside it to allow them a comfortable abode in our cells. However, let us not think that all the guile lies with the parasites while our immune system is just the fall guy.
   Our immune system, or earlier variants of it, has kept everyone of our ancestors alive to reproduce and by and large to provide nourishment and protection for themselves and at least some of their offspring. There must have been many times when they had to fight off potentially fatal infections: but equally there must have been many times when inconvenient IP could have rendered them ineffective in the face of perilous situations.
  An imperative for the immune system has been to allow our ancestors to be fit to meet the exigencies of life. Its mechanism is to avoid unnecessary IP. This it does by turning away from battles that don't need to be won, because the war is unlikely to be lost before the host can reproduce. This may not be completely suitable to us today, not octogenarians like me anyway: but we have to be happy that it got us here in the first place. And now we have Dr Marshall to help us when we have the luxury to survive despite the malaise of IP.

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I am continually in awe of what a healthy immune system can do. When I was in Shanghai, a one-inch gash was cut out of the top of my left foot by the door of the bathroom alcove at the hotel.

I applied antibiotic gel, and a 4x2 band-aid, and the next morning went to the CPhI conference, continually on my feet for 8 hours of solid walking.

That night there was some pus near the center of the gash, I cleaned the wound, applied some antibiotic gel again, and left the wound open overnight. I applied a 4x2 patch the next morning, and again the wound withstood 8 hours of constant walking inside my formal dress shoes...

Took the dressing off for the second night, and by the morning the wound looked good. I put a band-aid on it (the last large 4x2 inch patch in my traveling first-aid kit). Another day of walking, another night of healing, and I didn't even need any more band-aids or wound dressing.

My feet were in the same shoes without a break for 18 hours flying home that day, no problems.

I can remember when cuts used to take weeks to heal.. in fact, they have always taken weeks to heal, not 3 days...
 

eClaire
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Interesting Dr. Marshall.

Just like the cholesterol example above, unlike you, wounds always healed very quickly for me (super quickly).  I had bad acne as a teen as well and was not left with the terrible scars that others ended up with with similar problems.  And unlike many with immune issues, I did not seem to catch much of anything... never a cold and extremely few viruses.  Rather than look haggard and worn out, I look much younger than my years for the longest time.  My hair was lustrous and fast growing for years (though my nails were horrendous).

I know I am not alone in this--being very sick--but defying some of the things reported like those listed above.  I know I'm not alone because I've heard similar reports from others on the MP. 

Once again, this leads me back to how our microbiota determines much of these differences... just as it determines which disease label we get.

Jigsaw, your point is well taken.  I see a lot of wisdom in that.  Perhaps that might explain why the immune system down regulates during extreme stress (in the same way that bowels empty when people become very fearful).

Claire

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quorom sensing in tumours:

http://www.nature.com/bjc/journal/v100/n12/full/6605071a.html

http://www.economist.com/node/15268859

'What they do know is that when they grow these cells in culture, they can push them toward either asymmetrical or symmetrical division by controlling the density of cells and the amount of oxygen available.'

seanlane
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Of course....when I took Pamelor...a powerful Trycyclic anti-depressant that increases ephinephrine....I went manic and was hospitalized.

NickBowler
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'A mixture of just 10 nM of each amino acid is sufficient to disrupt biofilms'


http://pubs.acs.org/cen/news/88/i18/8818notw3.html


Prof Trevor Marshall
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By living inside the cytoplasm of living cells, the microbiota ensures that their environment is very carefully controlled (by the host).

Diesel
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TINKER, BACTERIA, EUKARYOTE, SPY

Bacteria and their hosts may reside in different kingdoms, but that doesn't stop them from intercepting each other's communications. Asher Mullard reports

http://www.nature.com/news/2009/090513/pdf/459159a.pdf

"Bacteria are conversing with us, and we're conversing with them," says Lyte. The question now is how to record more of the conversation — and work out what is being said. 

Regards,

Diesel

inuk2600
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One of the most universal and faithfully repeatable symptoms of CFS is post exertion malaise/fatigue. Most people with CFS would agree that you can replace the word exertion with any kind of stress in general. A flood of epinephrine always accompanies this exertion/stress. Could it be that this abnormal reaction (post exertion malaise) occurs somewhat directly from  a quorum-type response to epinephrine of certain intracellular bacteria species/combinations?


Last edited on Fri Oct 22nd, 2010 09:21 by inuk2600

Prof Trevor Marshall
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inuk2600 wrote: Could it be that this abnormal reaction (post exertion malaise) occurs somewhat directly from  a quorum-type response to epinephrine of certain intracellular bacteria species/combinations?
Most certainly :) This is indeed the best current explanation for why Th1 patients' bodies behave abnormally to epinephrine.
 

leroybrown
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I feel much better after exercising, but breaking through the pre-exertion malaise is the big problem for me.

Deb

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I am reading, for the first time in my life, about others who have a problem with epinephrine.  I am so grateful for this information.

I was unconscious at the dentist office - about 20 years ago - while having all of my old mercury fillings replaced with hypoallergenic material.  I was awakened by a sensation of my body having a massive earthquake.  It felt like my body was shaking violently while my heart raced out of control.  Although I was awake enough to realize all of this, I was not awake enough, at first, to open my eyes or to speak.  I was absolutely terrified.  I thought, "what is wrong with these people...can't they see that something is very wrong with me."  I thought this because they continued to work right along in my mouth as if nothing was amiss.  When I reached a point where I could open my eyes, my panic worsened as I looked down and realized that I was not moving, although the sensations of violent shaking from head to toe continued while my heart raced.  When I finally reached a point where I could speak and sit up, I shot up like an arrow, pushing these people back with my arm...almost knocking them to the floor.  Of course,  they were shocked that I would do such a thing.  I explained what I was feeling. The dentist called my neurologist and asked what was going on.  My neuologist asked what they had given me in the anaesthesia.  It was the epinephrine.  I had received a combination of carobaine, lidocaine, and epinephrine. 

I had a lot of auto antibodies to many of my own tissues.  My titer for anti-myelin antibodies was substantial and my neuro had previously diagnosed peripheral neuropathy, but he had never said anything about steering clear of epinephrine.  The point of this excerpt is this.  Tell your dentist, oral surgeon, peridontist, etc., to make a sign in big letters, "NO EPI" and place it on the inside front page of your file so everyone in the office will realize that you cannot have epi.  The last thing you need is to have a reaction like mine.  Of course, if you are ever taken to the ER in an unconscious state, you may get a shot of epinephrine, but, it is not necessary to use epinephrine at the dentist office... there are other substances that can be used.  

If this warning has been posted here or someplace else at this website, please forgive my intrusion and the use of your time to read this. 

Joyful
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Your story is not a new one, but it is worth retelling so that others are made aware of this.

It is addressed in the MP Knowledge Base here:
   Working with a dentist

minski2
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Hi Joyful......it may not be a new story,  but I have only run into one dentist that was aware of this and fortunately that was over 40 years ago.  I have moved often so I have had at least a dozen so called good dentists  I even had one dentist in Charlotte NC ignore my request not to use epi.....when I had a severe reaction he was as terrified as I was.  Should have sued!!!  We are so lucky to have this study site that affords us the opportunity to learn what is not common knowledge!!!!
  
Dian

inuk2600
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Moderate Exercise Increases Expression for Sensory, Adrenergic,
and Immune Genes in Chronic Fatigue Syndrome Patients
But Not in Normal Subjects


http://www.co-cure.org/Light.pdf

The mRNA was sampled from leukocytes.
The differences between the CFS group and healthy controls are interesting, especially the adrenergic function gene expression following exercise, ie. epinephrine dump. ;)


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Are you kidding???? Don't we already know from research cited here (somewhere) that the bacteria feed on epinephrine? Is that just the injected epinephrine that the dentists use, or is it the stuff we produce in our bodies as well?
Yikes. That's another good reason to avoid exercise until we've killed off a substantial amount of the bacteria (not that I have a choice anyway, since even small amounts of exertion trigger too much immune activity).
Marysue

eClaire
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Darn... whatever is killing me with this CFS definitely wants me to stay still.  Meanwhile, there are those running around telling me I need graded exercise.  Me?  I just want to do stuff.

Sallie Q
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Happy Christmas Claire
don't just do something
curl up with a good book ;-)
and a hopeful New Year to everybody
Sallie

Aunt Diana
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I have learned through trial and error over twenty years of Lyme and then 5 more years with Lyme + the MP....exercise will come back to BITE you every time. (At least it does come back and bite me...even the genlest form). Walking is about as far as I will go anymore and even then it is easy to overdo.
I know how frustrating this is since we all want to get back to what we were before we were ill, exerciise was so good for us. But, when one has neurological impairment, excercise will not rebuild muscle tone.
There are times one has no choice but to push oneself to get a necessary job done. I just came through such an ordeal when our shipping container with all or our world possessions arrived and we had a crew of 5 men who had two days to empty and sort and place furniture as well as possible. For two days, I had no choice but to muster all my strength and get the job done. (Frankly I was amazed at what I could get done....even the 5 stevadores were impressed with my energy).
That was 5 days ago and I am only now able to hobble around a bit...I have slept for the major part of the past 4 days and nights just recovering.)
Such is life...but it keeps getting better, slowly but surely.

HeatherK
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I too can still easily overdo it, in fact I just did... usually walking a few minutes a day is OK, but Saturday I went with my hubby  into the hill/field /woods across from us to cut some fir boughs and a christmas tree, Fun ! but the hill is steep, I was puffing in no time and did I ever pay up for that excursion, worst aches/pains in a year I think, especially hips and knees... 

we have medically proven reasons to be couch potatoes ? !!!  :D:D:D  

leroybrown
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I feel way better after I exercise (getting myself to DO it is the problem), but I can understand why people with certain diseases feel worse, especially in light of that study. Very interesting stuff.

Deb

JanEE
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Recently I thought I was doing fine by walking every other day or two, and it did make me feel better too.   I made it for about seven times in two and a half weeks or so, which is the longest I've been able to keep at it.  But once again I've had to stop.  There are so many of us that seem to react this way to exercise. 
 
I remember before beginning the MP I was taking lots of Aleve tablets trying to control the pain in my legs.  While it didn't totally do the job I sometimes wondered if underneath the masking of the pain I might be getting better and would slack off the Aleve slightly for a couple days.  I went through that many times, but always had to go back on all the pills.   Eventually though I discovered that I was able to take less of them, and finally, after a year or so, none.  So maybe it's sort of like that with the exercise.  We just have to keep trying every once in a while, and one day we'll find that we're able to keep at it longer and longer without crashing---and that will be the beginning of the good times.  That will be a day for rejoicing.

Marysue
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Jan,
I agree--and I do look forward to that day. ;):cool::D

inuk2600
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QseC Mediates Salmonella enterica Serovar Typhimurium Virulence In Vitro and In Vivo

http://iai.asm.org/cgi/content/full/78/3/914


"QseC plays a role in invasion of epithelial cells and intramacrophage survival."


inuk2600
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I haven't read the full text yet, but this looks interesting...

Targeting QseC Signaling and Virulence for Antibiotic Development


http://www.sciencemag.org/content/321/5892/1078.abstract

"Using a high-throughput screen, we identified a small molecule, LED209, that inhibits the binding of signals to QseC, preventing its autophosphorylation and consequently inhibiting QseC-mediated activation of virulence gene expression."





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