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Minocycline is an excellent Anti-inflammatory
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Prof Trevor Marshall
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 Posted: Mon Jul 23rd, 2012 11:26

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Mike, when one looks at the complexity of the human body with only historic pragma in one's eyes, it is easy to misinterpret what one sees. Indeed, 99% of the papers which cross my desk suffer from this problem. So I wouldn't get any more hung up about microglial activation than I would about 'vitamin D deficiency' :)

mvanwink5
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 Posted: Mon Jul 23rd, 2012 11:56

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Dr.Marshall,
Thanks, I took a look at some of what was written about the effect of Mino on microglial activation and it is much more complex than what "inhibition" might imply. Thanks and sorry for not looking into this further first.

Best regards,
Mike

Last edited on Mon Jul 23rd, 2012 12:19 by mvanwink5



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 Posted: Thu Nov 1st, 2012 03:48

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Minocycline modulates cytokine and chemokine production in lipopolysaccharide-stimulated THP-1 monocytic cells by inhibiting IκB kinase α/β phosphorylation.

http://www.ncbi.nlm.nih.gov/pubmed/23108365

Minocycline, which is a member of the broad-spectrum bacteriostatic tetracycline antibiotics group, has also recently been shown to have additional effects that are separate from their antimicrobial function; however, the detailed mechanisms involved remain unknown. We examined the effects of minocycline on cytokine and chemokine production and the expression levels of intracellular phosphorylated proteins in a lipopolysaccharide (LPS)-induced cytokine response model in vitro. In the present study, 3 cytokines (tumor necrosis factor [TNF]-α, interleukin [IL]-6, and interferon [IFN]-γ) and 7 chemokines (IL-8, interferon inducible protein [IP]-10, monocyte chemoattractant protein [MCP]-1, macrophage inflammatory protein [MIP]-1α, MIP-1β, regulated upon activation normal T-cell expressed secreted [RANTES], and eotaxin) were suppressed by minocycline in a dose-dependent manner. Moreover, the phosphorylation of inhibitor of nuclear factor-κB alpha (IκBα) and IκB kinase (IKK)α/β, which is located upstream from IκBα, was significantly suppressed by minocycline, whereas the phosphorylation of extracellular signal-regulated kinase (ERK)1/2, c-Jun N-terminal kinase (JNK), p38, and TGF-β-activated kinase (TAK)1 were not affected. Thus, minocycline appears to inhibit the signaling pathway at the level of IKKα/β phosphorylation. In conclusion, minocycline was found to reduce the production of multiple cytokines and chemokines by inhibiting LPS-induced IKKα/β phosphorylation. That is, minocycline appears to be a potent inhibitor of IKKα/β phosphorylation. From a clinical and translational significance point-of view, these findings suggest that the use of minocycline offers the advantage of providing both antimicrobial and anti-inflammatory effects, which may be key in treating certain types of infectious diseases, particularly those that lead to hypercytokinemia and chronic inflammatory disorders.

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 Posted: Thu Nov 1st, 2012 05:20

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Bane wrote: Minocycline modulates cytokine and chemokine production in lipopolysaccharide-stimulated THP-1 monocytic cells by inhibiting IκB kinase α/β phosphorylation.

http://www.ncbi.nlm.nih.gov/pubmed/23108365

Minocycline, which is a member of the broad-spectrum bacteriostatic tetracycline antibiotics group, has also recently been shown to have additional effects that are separate from their antimicrobial function; however, the detailed mechanisms involved remain unknown. We examined the effects of minocycline on cytokine and chemokine production and the expression levels of intracellular phosphorylated proteins in a lipopolysaccharide (LPS)-induced cytokine response model in vitro. In the present study, 3 cytokines (tumor necrosis factor [TNF]-α, interleukin [IL]-6, and interferon [IFN]-γ) and 7 chemokines (IL-8, interferon inducible protein [IP]-10, monocyte chemoattractant protein [MCP]-1, macrophage inflammatory protein [MIP]-1α, MIP-1β, regulated upon activation normal T-cell expressed secreted [RANTES], and eotaxin) were suppressed by minocycline in a dose-dependent manner. Moreover, the phosphorylation of inhibitor of nuclear factor-κB alpha (IκBα) and IκB kinase (IKK)α/β, which is located upstream from IκBα, was significantly suppressed by minocycline, whereas the phosphorylation of extracellular signal-regulated kinase (ERK)1/2, c-Jun N-terminal kinase (JNK), p38, and TGF-β-activated kinase (TAK)1 were not affected. Thus, minocycline appears to inhibit the signaling pathway at the level of IKKα/β phosphorylation. In conclusion, minocycline was found to reduce the production of multiple cytokines and chemokines by inhibiting LPS-induced IKKα/β phosphorylation. That is, minocycline appears to be a potent inhibitor of IKKα/β phosphorylation. From a clinical and translational significance point-of view, these findings suggest that the use of minocycline offers the advantage of providing both antimicrobial and anti-inflammatory effects, which may be key in treating certain types of infectious diseases, particularly those that lead to hypercytokinemia and chronic inflammatory disorders.

  These effects are consistent with an action through SOCS-1 (suppressor of cytokine signalling-1). Suppressor of Cytokine Signaling (SOCS) 1 Inhibits Type I Interferon (IFN) Signaling via the Interferon α Receptor (IFNAR1)-associated Tyrosine Kinase Tyk2

SOCS-1 is reported to be induced by activation of PXR.  Modulation of T Lymphocyte Function by the Pregnane X Receptor -- Dubrac et al. 184 (6): 2949 -- The Journal of Immunology

Last edited on Thu Nov 1st, 2012 05:23 by Jigsaw



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 Posted: Thu Nov 1st, 2012 05:26

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Jigsaw wrote:

  These effects are consistent with an action through SOCS-1 (suppressor of cytokine signalling-1). Suppressor of Cytokine Signaling (SOCS) 1 Inhibits Type I Interferon (IFN) Signaling via the Interferon α Receptor (IFNAR1)-associated Tyrosine Kinase Tyk2

SOCS-1 is reported to be induced by activation of PXR.  Modulation of T Lymphocyte Function by the Pregnane X Receptor -- Dubrac et al. 184 (6): 2949 -- The Journal of Immunology

You're called Jigsaw for a reason ;)



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Bane
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 Posted: Fri Nov 30th, 2012 07:34

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Minocycline blocks asthma-associated inflammation in part by interfering with the T Cell receptor-NF-κB-GATA-3-IL-4 axis without a prominent effect on PARP.

http://www.jbc.org/content/early/2012/11/26/jbc.M112.419580.long

Minocycline protects against asthma independently of its antibiotic function and was recently reported as a potent PARP inhibitor. In an animal model of asthma, a single administration of minocycline conferred excellent protection against ovalbumin-induced airway eosinophilia, mucus hypersecretion, and Th2 cytokine production (IL-4/IL-5/IL-12(p70)/IL-13/GM-CSF) and a partial protection against airway hyperresponsiveness. These effects correlated with pronounced reduction in lung and sera allergen-specific IgE. A reduction in poly(ADP-ribose)-immunoreactivity in lungs of minocycline-treated/ovalbumin-challenged mice correlated with decreased oxidative DNA damage. Minocycline's effect on PARP may be indirect as the drug failed to efficiently block direct PARP activation in lungs of N-methyl-N'-nitro-N-nitroso-guanidine-treated mice or H2O2-treated cells suggesting. Minocycline blocked allergen-specific IgE production in B cells potentially by modulating T cell-receptor (TCR)-linked IL-4 production at the mRNA level but not through a modulation of the IL-4-JAK-STAT-6 axis, IL-2 production, or NFAT1 activation. Restoration of IL-4, ex vivo, rescued IgE production by minocycline-treated/ovalbumin-stimulated B cells. IL-4 blockade correlated with a preferential inhibition of the NF-κB activation arm of TCR but not GSK3, Src, p38 MAPK, or ERK1/2. Interestingly, the drug promoted a slightly higher Src and ERK1/2 phosphorylation. Inhibition of NF-κB was linked to a complete blockade of TCR-stimulated GATA-3 expression, a pivotal transcription factor for IL-4 expression. Minocycline also reduced TNF-α-mediated NF-κB activation and expression of dependent genes. These results show a potentially broad effect of minocycline but may block IgE production in part by modulating TCR function particularly by inhibiting the signaling pathway leading to NF-κB activation, GATA-3 expression, and subsequent IL-4 production.


http://en.wikipedia.org/wiki/Interleukin_4

Functions
 
It has many biological roles, including the stimulation of activated B-cell and T-cell proliferation, and the differentiation B cells into Plasma Cells.
 
It is a key regulator in humoral and adaptive immunity.
 
IL-4 induces B-cell class switching to IgE, and up-regulates MHC class II production. It also induces B cell class switching to IgG4.
 
IL-4 decreases the production of Th1 cells, macrophages, IFN-gamma, and dendritic cell IL-12.
 
Overproduction of IL-4 is associated with allergies.

Last edited on Fri Nov 30th, 2012 07:52 by Bane

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 Posted: Sat Dec 29th, 2012 07:39

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Does minocycline have antidepressant effect?



@duke.edu
Abstract
Only one-third of patients undergoing monotherapy with an antidepressant achieve remission of their depressive symptoms and gain functional recovery. Therefore, further exploration of antidepressant mechanisms of action is important in order to facilitate the development of antidepressants with new modes of action. Preclinical and clinical studies have demonstrated that major depression is associated with impaired inflammatory responses and deficient neuroprotection. In this regard, we propose that the second-generation tetracycline "minocycline" may hold a potential as a new treatment for major depression. Emerging findings in animal and human studies of minocycline reveal that it has antidepressant-like neuroprotective and anti-inflammatory actions, and minocycline has been shown to perform as an antidepressant in an accepted animal model (forced swimming test). Anecdotal evidence supports minocycline's efficacy for augmentation of antidepressants in major depressive disorder. The following review describes the evidence supporting the consideration of minocycline as a potential antidepressant. We suggest that minocycline may be particularly helpful in patients with depression and comorbid cognitive impairment, as well as depression associated with organic brain disease. We also describe the antinociceptive effect of minocycline and propose a role for minocycline in the treatment of patients with major depression and prominent somatic discomfort and somatoform spectrum disorders. The lack of clinical studies of minocycline for depression is noted. Further studies of the potential therapeutic mechanism of minocycline and its therapeutic implications for major depression are warranted, and may substantially contribute to the development of newer and more effective antidepressants.



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 Posted: Sat Dec 29th, 2012 17:55

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Sean,

I always have more motivation/desire to do things the day after I have taken a 100mg mino the previous evening. I would consider the effect it has on me as mildly anti-depressive (although I do not suffer from major depression or any officially diagnosed depression for that matter).



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 Posted: Sat Dec 29th, 2012 20:18

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Yes...I find the same thing.



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 Posted: Mon Dec 31st, 2012 09:03

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This is very interesting indeed.  Perhaps I could use mino instead of the AD I currently take.  I'll have to talk this one over with my MP doc.



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 Posted: Thu Mar 28th, 2013 01:54

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A minocycline derivative reduces nerve injury-induced allodynia, LPS-induced prostaglandin E2 microglial production and signaling via toll-like receptors 2 and 4.

http://www.ncbi.nlm.nih.gov/pubmed/23523650

Many studies have shown that minocycline, an antibacterial tetracycline, suppresses experimental pain. While minocycline's positive effects on pain resolution suggest that clinical use of such drugs may prove beneficial, minocycline's antibiotic actions and divalent cation (Ca2+; Mg2+) chelating effects detract from its potential utility. Thus, we tested the antiallodynic effect induced by a non-antibacterial, non-chelating minocycline derivative in a model of neuropathic pain and performed an initial investigation of its anti-inflammatory effects in vitro. Intraperitoneal minocycline (100 mg/kg) and 12S-hydroxy-1,12-pyrazolinominocycline (PMIN; 23.75 mg/kg, 47.50 mg/kg or 95.00 mg/kg) reduce the mechanical allodynia induced by chronic constriction injury of mouse sciatic nerve. PMIN reduces the LPS-induced production of PGE2 by primary microglial cell cultures. Human embryonic kidney cells were transfected to express human toll-like receptors 2 and 4, and the signaling via both receptors stimulated with PAM3CSK4 or LPS (respectively) was affected either by minocycline or PMIN. Importantly, these treatments did not affect the cell viability, as assessed by MTT test. Altogether, these results reinforce the evidence that the anti-inflammatory and experimental pain suppressive effects induced by tetracyclines are neither necessarily linked to antibacterial nor to Ca2+ chelating activities. This study supports the evaluation of the potential usefulness of PMIN in the management of neuropathic pain, as its lack of antibacterial and Ca2+ chelating activities might confer greater safety over conventional tetracyclines.

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 Posted: Thu Mar 28th, 2013 04:20

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So, are they saying that minocycline reduced both expression and signaling of TLR2 and TLR4? Sometimes I have trouble understanding researcher language. (I would have read the paper to illuminate what was being said but all I could read was the abstract).

Last edited on Thu Mar 28th, 2013 04:23 by mvanwink5



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mvanwink5
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 Posted: Thu Mar 28th, 2013 07:16

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Ok, got the paper, thank you. First, it is a murine study, so I don't know what it means to humans, but for the mice, "Minocycline or PMIN inhibits also TLR2 and TLR4 signaling. TLRs are transmembrane pattern-recognition receptors, which respond to both exogenous and endogenous ligands. The exogenous ligands that are mainly recognized by TLR2 are lipoproteins from gram-positive bacteria, whereas TLR4 recognizes predominantly endotoxin (LPS) from gram-negative bacteria."

(bolding added)



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 Posted: Thu Mar 28th, 2013 07:43

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which for us dummies means what?  Is it palliative or is it killing bugs?  For me it appears to be palliative.  I take it when my pain becomes too intense, but I never have been able to figure out whether my intense pain was IP or my Lyme!?  Any ideas?

Dian



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Prof Trevor Marshall
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 Posted: Thu Mar 28th, 2013 11:15

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In my last webconference I explained why its concentration inside the cells did not reach levels which would kill many bugs... Nice to have the study supporting my own conclusions, however...

Knocking out TLR2 and TLR4, if it is repeated in humans, would most definitely be palliative as it would significantly knock-down intraphagocytic innate immunity.

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 Posted: Thu Mar 28th, 2013 12:08

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Thanks Dr. Marshall.......



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Jigsaw
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 Posted: Thu Mar 28th, 2013 17:59

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Bane wrote: A minocycline derivative reduces nerve injury-induced allodynia, LPS-induced prostaglandin E2 microglial production and signaling via toll-like receptors 2 and 4.

http://www.ncbi.nlm.nih.gov/pubmed/23523650
  Intraperitoneal minocycline (100 mg/kg) and 12S-hydroxy-1,12-pyrazolinominocycline (PMIN; 23.75 mg/kg, 47.50 mg/kg or 95.00 mg/kg) reduce the mechanical allodynia induced by chronic constriction injury of mouse sciatic nerve. PMIN reduces the LPS-induced production of PGE2 by primary microglial cell culture

   Could PMIN be a PXR agonist like mino?



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 Posted: Fri Apr 12th, 2013 06:45

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A Randomized Double-Blind, Placebo-Controlled Trial of Minocycline in Children and Adolescents with Fragile X Syndrome.

http://www.ncbi.nlm.nih.gov/pubmed/23572165

OBJECTIVE:: Minocycline rescued synaptic abnormalities and improved behavior in the fragile X mouse model. Previous open-label human studies demonstrated benefits in individuals with fragile X syndrome (FXS); however, its efficacy in patients with FXS has not been assessed in a controlled trial. METHOD:: Randomized, double-blind, placebo-controlled, crossover trial in individuals with FXS, aged 3.5 years to 16 years (n = 55, mean age 9.2 [SD, 3.6] years). Participants were randomized to minocycline or placebo for 3 months and then switched to the other treatment. RESULTS:: Sixty-nine subjects were screened and 66 were randomized. Fifty-five subjects (83.3%) completed at least the first period and 48 (72.7%) completed the full trial. Intention-to-treat analysis demonstrated significantly greater improvements in one primary outcome, Clinical Global Impression Scale-Improvement after minocycline compared with placebo (2.49 ± 0.13 and 2.97 ± 0.13, respectively, p = .0173) and greater improvement in ad hoc analysis of anxiety and mood-related behaviors on the Visual Analog Scale (minocycline: 5.26 cm ± 0.46 cm, placebo: 4.05 cm ± 0.46 cm; p = .0488). Side effects were not significantly different during the minocycline and placebo treatments. No serious adverse events occurred on minocycline. Results may be potentially biased by study design weaknesses, including unblinding of subjects when they completed the study, drug-related side effects unblinding, and preliminary efficacy analysis results known to investigators. CONCLUSIONS:: Minocycline treatment for 3 months in children with FXS resulted in greater global improvement than placebo. Treatment for 3 months appears safe; however, longer trials are indicated to further assess benefits, side effects, and factors associated with a clinical response to minocycline.

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 Posted: Sat Apr 20th, 2013 03:07

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Bane wrote:
Bane wrote:Does minocycline, an antibiotic with inhibitory effects on microglial activation, sharpen a sense of trust in social interaction?

http://www.ncbi.nlm.nih.gov/pubmed/21956241

METHODS:Forty-nine healthy volunteers were administered minocycline or placebo over four days, after which they played (1) a trust game, in which they decided how much to trust an anonymous partner, and (2) a dictator game, in which they decided how to divide resources between themselves and an anonymous partner.

CONCLUSIONS:These results suggest that minocycline led to more rational decision-making strategies, possibly by increasing emotion regulation. Since minocycline is a well-known inhibitor of microglial activation, our findings may open a new optional pathway for treating mental states in which a component of rational decision making is impaired.

Minocycline modulates human social decision-making: possible impact of microglia on personality-oriented social behaviors.

http://www.ncbi.nlm.nih.gov/pubmed/22808165

CONCLUSIONS/SIGNIFICANCE: Our results suggest that minocycline led to more situation-oriented decision-making, possibly by suppressing the effects of personality traits, and furthermore that personality and social behaviors might be modulated by microglia. Early-life events may activate human microglia, establish a certain neuro-synaptic connection, and this formation may determine each human's personality and personality- oriented social behaviors in later life. To explore these mechanisms, further translational research is needed.





Minocycline, a microglial inhibitor, reduces ‘honey trap’ risk in human economic exchange :D

http://www.nature.com/srep/2013/130418/srep01685/full/srep01685.html

Recently, minocycline, a tetracycline antibiotic, has been reported to improve symptoms of psychiatric disorders and to facilitate sober decision-making in healthy human subjects. Here we show that minocycline also reduces the risk of the ‘honey trap’ during an economic exchange. Males tend to cooperate with physically attractive females without careful evaluation of their trustworthiness, resulting in betrayal by the female. In this experiment, healthy male participants made risky choices (whether or not to trust female partners, identified only by photograph, who had decided in advance to exploit the male participants). The results show that trusting behaviour in male participants significantly increased in relation to the perceived attractiveness of the female partner, but that attractiveness did not impact trusting behaviour in the minocycline group. Animal studies have shown that minocycline inhibits microglial activities. Therefore, this minocycline effect may shed new light on the unknown roles microglia play in human mental activities.

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 Posted: Sat Apr 20th, 2013 08:17

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I read this and immediately thought of cats and mice and toxoplasmosis.  Mice infected with toxoplasmosis will run TOWARDS a cat rather than away. 

I wonder if they will try a design a similar experiment for women and mino, but what would the "honey trap" be?  Shoes?  Do you trust these shoes?  Or will you, after mino, recognize that they will kill your feet? Inquiring minds want to know.



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