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Anti-inflammatory and other positive effects of antibiotics

Discussion in 'Antivirals, Antibiotics and Immune Modulators' started by guest, Feb 19, 2011.

  1. guest

    guest Guest

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    We often hear about how bad antibiotics are for us. That's why I found it very interesting to read about the many positive effects antibiotics can have, besides destroying bacteria.

    http://www.aldf.com/Book_Review_on_Antibiotics_as_inflamatory_agents.pdf

    Abilities (1) to suppress the expression of virulence factors (e.g., quorum sensing mechanisms, as well as the production of exotoxins, exopolysaccharides, pili, flagellin, and lipopolysaccharides);
    (2) to accumulate in in-flammatory cells in high concentration, thereby providing more efficient deliveryof antibiotic to sites of infection;
    (3) to downregulate the molecular expression of integrins known to influence leukocyte
    adhesion and the accumulation of macrophages and neutrophils at sites of infection; (4) to inhibit the maturation and proliferation of subsets of T lymphocytes,
    as well as to influence immunoglobulin secretion and isotype class switching by B
    lymphocytes;
    (5) to protect the respiratoryciliated epithelium from bacterial injury
    by interfering with bacterial adherenceand colonization;
    (6) to inhibit neutrophil migration;
    (7) to modulate the expression of adhesion molecules and to reduce the
    production of chemotactic factors at the site of inflammation;
    (8) to increase the
    production of various inflammatory cytokines (IL-8, IL-1b, and TNF-a) that are
    potent activators of neutrophils;
    (9) to increase the production of IL-2, colony stimulating factor, and other cytokines that modulate the induction of TH1 and TH2
    lymphocyte activity; and
    (10) to cause significant reductions in the number of lymphocytes and the ratio of CD4+CD8+T lymphocytes.

    The clinical implications of some of these effects are discussed with reference
    to which antibiotics are used as mucoregulatory agents for treating diffuse panbronchiolitis, cystic fibrosis, various upper airway diseases, chronic asthma, and lung injury, as well as which antibiotics are used for the development of more precise therapies to prevent biofilm diseases or chronic inflammation without increasing
    the risk of antimicrobial resistance to macrolides. The implications of these findings
    with respect to protracted antibiotic therapy remain to be fully assessed. If one also
    considers the results of a recent study [1] that indicates that as many as 15 different
    b-lactam antibiotics, including penicillin and its derivatives, exert profound neuroprotective effects, it, indeed, may be difficult at times to attribute the beneficial
    effects antibiotic therapy to any particular mechanism.


    http://jpet.aspetjournals.org/content/292/1/156.full

    In conclusion, the present study shows that macrolide antibiotics have anti-inflammatory activity, which likely depends on their ability to prevent the production of proinflammatory mediators and cytokines, and suggests that these agents, particularly roxithromycin, can exert therapeutic effects independent of their antibacterial activity.
  2. guest

    guest Guest

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    Asthma Tied to Bacterial Communities in the Airway

    http://www.sciencedaily.com/releases/2011/02/110217151457.htm

    ScienceDaily (Feb. 19, 2011) — Asthma may have a surprising relationship with the composition of the species of bacteria that inhabit bronchial airways, a finding that could suggest new treatment or even potential cures for the common inflammatory disease, according to a new UCSF-led study.

    Using new detection methods, researchers learned that the diversity of microbes inside the respiratory tract is far vaster than previously suspected -- creating a complex and inter-connected microbial neighborhood that appears to be associated with asthma, and akin to what has also been found in inflammatory bowel disease, vaginitis, periodontitis, and possibly even obesity.
    Contrary to popular belief, the scientists also learned that the airways are not necessarily entirely sterile environments, even in healthy people, while the airways of asthmatics are infected by a richer, more complex collection of bacteria. These findings could improve understanding of the biology of asthma, and potentially lead to new and much-needed therapies.
    "People thought that asthma was caused by inhalation of allergens but this study shows that it may be more complicated than that -- asthma may involve colonization of the airways by multiple bacteria,'' said study co-author Homer Boushey, MD, a UCSF professor of medicine in the division of Pulmonary and Critical Care Medicine.
    The study is published online in the Journal of Allergy and Clinical Immunology.
    Asthma is one of the most common diseases in the world, with approximately 300 million asthmatics globally, including 24 million in the United States, according to the Centers for Disease Control. The disease has been on the rise for the last 60 years.
    "It has gone from 3 percent of the population to slightly more than 8 percent of the population in the U.S.,'' said Boushey. "It is most prevalent in western, developed nations -- and we don't know why.''
    In recent years, scientists began studying communities of mixed-species microorganisms (microbiome) found in both diseased and healthy people to better understand their role in a variety of diseases. But research on the microbiome in respiratory disease is relatively uncharted terrain.
    "We know fairly little about the diversity, complexity and collective function of bacteria living in the respiratory tract, and how they might contribute to diseases like asthma,'' said Yvonne J. Huang, MD, the paper's first author. She is a research fellow and clinical instructor in the UCSF Pulmonary Division.
    "Traditionally, the airways have been thought to be sterile. However, this study suggests this is not the case. Certain asthma patients who require inhaled corticosteroid therapy possess a great abundance of bacteria compared to healthy individuals, and have an increased relative abundance of specific organisms that is correlated with greater sensitivity of their airways.''
    In their three-year pilot project, the scientists collected samples from the airway linings of 65 adults with mild to moderate asthma and 10 healthy subjects. Then, using a tool that can identify approximately 8,500 distinct groups of bacteria in a single assay, the scientists profiled the organisms present in each sample to look for relationships between bacterial community composition and clinical characteristics of the patients' asthma.
    The researchers found that bronchial airway samples from asthmatic patients contained far more bacteria than samples from healthy patients. The scientists also found greater bacterial diversity in the asthmatic patients who had the most hyper-responsive or sensitive airways (a feature of asthma).
    "People have viewed asthma as a misdirected immune reaction to environmental exposures, but few have thought of it in the context of airway microbiota composition,'' said senior author Susan Lynch, PhD, an assistant professor of medicine and director of the UCSF Colitis and Crohn's Disease Microbiome Research Core in the division of gastroenterology.
    "We took an ecological approach, considering the bacteria in the context of their microbial neighborhoods to identify relationships between characteristics of these communities and features of the disease…This new approach will help us to better understand the microbiota-host relationships that define human health.''
    The authors say that further studies are needed to determine how these specific bacteria identified in the study may influence the cause and development of asthma.
    ###
    The study was supported by the National Heart, Lung and Blood Institute and by the Strategic Asthma Basic Research Center at UCSF, supported by the Sandler Family Foundation. Huang was funded by a National Institutes of Health grant and by a UC Tobacco-related Disease Research Program award; Lynch receives research support from the NIH; Boushey is an ad-hoc consultant for KaloBios Pharmaceuticals, Inc., is on the advisory committee for Pharmaxis, is on ad-hoc advisory committees for GlaxoSmithKline and Merck, and receives research support from GlaxoSmithKline.
    UCSF is a leading university dedicated to promoting health worldwide through advanced biomedical research, graduate-level education in the life sciences and health professions, and excellence in patient care.

    http://www.bentham.org/cmp/samples/cmp 1-1/Nau.pdf

    The immunomodulatory and neuroprotective effects of
    tetracyclines – especially minocycline – in neurological diseases are considered to be due in part to the suppression of
    microglia activation. To further illuminate the molecular
    signal transduction pattern resulting in an inhibition of microglia activation in vitro, rat microglial and neuronal cells
    were pre-treated with 10 microM minocycline or doxycycline and then exposed to hypoxia. Both antibiotics suppressed microglia activation as assessed by Iba1 (ionized
    calcium-binding adaptor molecule 1) staining and activation
    of ED1, a membrane-bound lysosomal glycoprotein, both
    markers for microglial activation. This effect was accompanied by down-regulation of pro-inflammatory molecules
    such as NO, IL-1 and TNF-. In contrast, tetracycline
    treatment did not increase the concentrations of neuroprotective proteins such as brain-derived neurotrophic factor
    (BDNF) or glial cell line-derived neurotrophic factor
    (GDNF). From these results the authors concluded that neuroprotection presumably is achieved by the regulation of
    microglial activity and not by changes in microglia proliferation or viability [12].
  3. Mya Symons

    Mya Symons Mya Symons

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    When I was in the hospital on I.V. antibiotics for the first time in years I had no pain, eventhough I had a bad post-operative infection. I guess that is an indicator of how bad our pain is. For awhile I got my hopes up that I had actually had some kind of all over bacteria infection and I really did not have CFS or FMS. However, as soon as I got off thos I.V. antibiotics the pain came back. I think now that it was due to the anti-inflammatory properties of the antibiotics I was on. I thought about doing the Marshall protocol just for the anti-inflammatory effects of the antibiotics. Taking antibiotics too long can come with some nasty life threatening side effects like pseudomembranous colitis, but I might just take the risk. Being out of pain for a couple days felt so great. (I did not have pain killers in the hosptial because I kept on vomitting and asked the nurses to take me off the pain killers.)
  4. kday

    kday Senior Member

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    I'm not sure why people here assume they don't have bacterial infections.

    Many of my RBCs and most of my WBCs were filled with intracellular bacteria resembling the shape of L-Forms. You need a dark field microscope to see.

    A macrolide (and most other antibiotics) aren't going to kill the bacteria that are in cell wall deficient form, and many antibiotics used aren't intracellular. For survival, bacteria may shift to L-Form in presence of antibiotics.

    I haven't checked in a while, but with treatment, I can find them anymore on a smear.

    An immunocompetent patient can probably get rid of the infection on their own after the bacteria with a cell wall are killed. I wouldn't consider people with CFS in this category.
  5. Mya Symons

    Mya Symons Mya Symons

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    kday, I was on about 7 or 8 different antibiotics while I was in the hospital. The first batch did not work. I am curious if one of the antibiotics they put me on is one that could kill the L-Form bacteria you are writing about. Do you know the names of the antibiotics that kill L-form bacteria?
  6. ggingues

    ggingues $10 gift code at iHerb GAS343 of $40

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    Thanks for the postings that you do Diesel, but is there any chance that you could space out the info? It's all like one huge paragraph which makes it very hard to read!

    Thanks!!

    GG
  7. heapsreal

    heapsreal iherb 10% discount code OPA989,

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    azithromycin was one abx that was studied in cfs and shown to have anti-inflammatory/immunomodulating effects. Had had some good response from doxycyline years ago but had to go through a die off type reaction for a few weeks before i felt any better but progress stalled from there .
  8. kday

    kday Senior Member

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    Did any of the antibiotics make you feel worse? This is the usual pattern in my opinion.

    In a short course, I think it's possible for Rocephin to make you feel better. In fact, many initially feel a lot better. But I think this may be more from suppression of glutamate in the brain than direct anti-inflammtory effects. Of course, it's probably a combination of both, but i lean more towards to glutamate suppression theory. A lot of literature avoids talking about this for some reason, but it has been studied on ALS patients. I think other cephalosporins may have similar action.

    I wonder if you had Rocephin or another IV cephalosporin.

    You aren't going to get Roxithromyocin unless you live in Europe.
  9. knackers323

    knackers323 Senior Member

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    i have taken klacid before and after one day I felt that I had found 'the cure'. i continued to feel good while I was on them but went strait back down once I stopped. docs have said that it was probably due to the anti-inflamitory effects, so I asked for something that would have the same effect but was told that antibiotics are the only things that work on inflamation this way. does anyone know if that is true or was he just brushing me off?
  10. kday

    kday Senior Member

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    Doctors make way too many assumptions. And if they don't understand you can harbor chronic viral and bacterial infections because of an immunodeficiency that you may have, I guess the easy assumption is that it must be anti-inflammatory effects.

    I am skeptical of it being strictly an anti-inflammatory effect especially since it felt like you found a cure, but what do I know, I am not a doctor.
  11. pine108kell

    pine108kell Senior Member

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    Every time this topic comes up, I chime in because antibiotics have such a profound and complex effect on me and it is almost impossible for me to get me doctor to understand this.

    First, there is no doubt that the direct effect of antibiotics are anti-inflammatory for me. When I first take them, I immediately feel much better--reduced brain problems, OI/POTS etc. If I could maintain this affect, my life would be 30-40% improved. I can actually write paragraphs etc., without getting aggitated and dysfunctional. I can stand up much easier.

    However, I also have chronic infections, probably including lyme. Because of this, I start feeling much worse after a day or so because of die-off. Eventually I become a complete basketcase from all the die off and inflammation actually increases.

    Even if I did not get the die off reaction, I would probably not take antibiotics every day my whole life. However, for me, someone needs to find a drug with the anti-inflammatory properties of antibiotics without the real purpose of antibiotics (killing bacteria) and other side effects, including the killing of gut bacteria.

    I think my periodic use of antibiotics has suppressed infections some, but I think anyone with CFS that feels much better after just a short course of antibiotics is only experiencing the anti-inflammatory aspect. I would not suggest, however, that this means that they definitely do not have chronic bacterial infections.
  12. cigana

    cigana Senior Member

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    I will add my experiences. Antibiotics make me feeel a lot better. I think it is the anti-inflammatory effects, because it kicks in after about 8 hours, which I assume is too soon to kill a good fraction of any bacterial infection. It has to be quite high doses though - 500mg a day did nothing, but 3g a day was great (Amoxicillin). I was able to walk for 2 hours and then not crash.

    So I do not believe at all when they tell us there are no drugs that work for CFS. Antibiotics for me improve every symptom significantly. It will be really interesting when this site gets its patient data repository up and working to see how many patients benefit.

    Cheers for starting the thread Diesel,

    Marke
  13. energyoverload

    energyoverload

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    If you want to try and gain the anti-inflammatory benefits that antibiotics give with out the bacteria killing aspect that causes die off problems etc. for many, have you heard of Benicar (Olmesartan)? It has been found to have anti-inflammatory action through inhibition of Nf-Kb - a gene that regulates cytokine production. It is also used in the marshall protocol and it is suspected that some of the imporvement people get is through its anti inflammatory actions.
  14. pine108kell

    pine108kell Senior Member

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    Yes, an interesting suggestion. I have tried Benicar and agree that is does definitely reduce inflammation, at least in the short term. No question about it, I felt much better for a few days on it. However, after 3-4 days I started feeling much worse to the point of intolerance (different than antibiotics or oxygen). At that time, "Dr." Marshall and his group were providing all kinds of theories why this reaction was happening, but none of them really made sense.

    I think Benicar is one of those drugs that could be useful for us, but we really need some clinical studies on what the long term effects are for those with CFS. Benicar is a cheap, fully developed drug. It seems to me that these kinds of studies would not be expensive but no one ever bothers, so we are just left with anecdotes and what "Dr." Marshall says is true.
  15. Mya Symons

    Mya Symons Mya Symons

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    I just realized that Ceftriaxone is Rocephin. Yes, that was one of the main antibiotics I had. None of them made me worse, but some made me somewhat nauseous.
  16. glenp

    glenp "and this too shall pass"

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    I was on minocycline for 6 months - I stopped about 2 months ago - it really helped my head pain, migraines, non existent smells, soar throat, and ability to add numbers- I am still better but have had to take some migraine meds. The buzzing in my ears got worse so I stopped. I may try pulsing at a later date. Minocycline is one of the antibiotics prescribed by a physician here who follows the Marshall protocol

    Many years ago i was on various IV antibiotics for 6 months - felt good after that
    There has been interesting research on minocycline helping those with HIV - google "minocycline hiv"

    http://www.suite101.com/content/hiv-prevention-through-an-acne-drug-a217324

    http://jid.oxfordjournals.org/content/201/8/1132.full

    "Minocycline reduces the capability of the virus to emerge from resting infected T-cells," Szeto added. "It prevents the virus from escaping in the one in a million cells in which it lays dormant in a person on [combination ART], and since it prevents virus activation it should maintain the level of viral latency or even lower it. That's the goal: Sustaining a latent non-infectious state."


    glen
  17. Mya Symons

    Mya Symons Mya Symons

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    That's interesting. I wonder if minocycline would interfere with XMRV replication in some way? I remember reading about mycoplasma and minocycline in HIV patients. They are susceptible to getting mycoplasma infections in the brain which causes all kinds of neurological problems. They used minocycline to keep the mycoplasma infections controlled.
  18. energyoverload

    energyoverload

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    that's interesting about minocycline maintaining hiv latency.

    out of interest has anyone tried any of the TNf-a inhibitor type drugs - commonly used in Rheumatoid arthritis, chrons etc.?

    It seems like cytokine modulation is key here.
  19. physicsstudent13

    physicsstudent13 Senior Member

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    I tried 6 weeks of azithromycin and it was a terrible disaster, a couple of months after I couldn't exhale well and have airway resistance now. do these antibiotic treatments work? some people say they are quackery- isn't asthma mainly an inflammatory process instead of infectious? I was looking into taking xolair since my IGE is high and started allergy shots but couldn't resume them lately
  20. yarnee

    yarnee

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    I would hate to be on antibiotics more than brief period it has a lot of damaging things to the body.

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