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Even Bacteria get lonely
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Prof Trevor Marshall
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 Posted: Sun Apr 4th, 2010 14:04

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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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 Posted: Sun Apr 4th, 2010 16:55

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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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 Posted: Sun Apr 4th, 2010 17:26

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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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 Posted: Sun Apr 4th, 2010 18:57

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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



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Prof Trevor Marshall
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 Posted: Mon Apr 5th, 2010 03:18

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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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 Posted: Mon Apr 5th, 2010 08:17

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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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 Posted: Mon Apr 5th, 2010 12:12

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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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 Posted: Mon Apr 5th, 2010 22:14

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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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 Posted: Mon Apr 5th, 2010 22:20

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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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 Posted: Tue Apr 6th, 2010 08:34

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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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 Posted: Tue Apr 6th, 2010 09:09

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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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 Posted: Tue Apr 6th, 2010 12:18

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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



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 Posted: Tue Apr 6th, 2010 13:48

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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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 Posted: Tue Apr 6th, 2010 18:54

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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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 Posted: Wed Apr 7th, 2010 12:49

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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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 Posted: Thu Apr 8th, 2010 17:51

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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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 Posted: Thu Apr 8th, 2010 21:02

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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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 Posted: Thu Apr 8th, 2010 23:15

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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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 Posted: Fri Apr 9th, 2010 20:27

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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



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 Posted: Sat Apr 10th, 2010 18:45

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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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