N-Acetylglucosamine Prevents IL-1β-Mediated Activation in ME/CFS...

Discussion in 'Fibromyalgia Main Forum' started by RadioFM, Mar 10, 2015.

  1. RadioFM

    RadioFM Active Member

    Evidence for inflammation and activation of cell-mediated immunity in Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS): increased interleukin-1, tumor necrosis factor-α, PMN-elastase, lysozyme and neopterin.


    "There is evidence that inflammatory pathways and cell-mediated immunity (CMI) play an important role in the pathophysiology of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS). Activation of inflammatory and CMI pathways, including increased levels of cytokines, is known to induce fatigue and somatic symptoms. Given the broad spectrum inflammatory state in ME/CFS, the aim of this study was to examine whether inflammatory and CMI biomarkers are increased in individuals with ME/CFS."


    "In this study we therefore measured plasma interleukin-(IL)1, tumor necrosis factor (TNF)α, and PMN-elastase, and serum neopterin and lysozyme in 107 patients with ME/CFS, 37 patients with chronic fatigue (CF), and 20 normal controls. The severity of ME/CFS was measured with the Fibromyalgia and Chronic Fatigue Syndrome (FF) Rating Scale."


    "Serum IL-1, TNFα, neopterin and lysozyme are significantly higher in patients with ME/CFS than in controls and CF patients. Plasma PMN-elastase is significantly higher in patients with ME/CFS than in controls and CF patients and higher in the latter than in controls. Increased IL-1 and TNFα are significantly correlated with fatigue, sadness, autonomic symptoms, and a flu-like malaise; neopterin is correlated with fatigue, autonomic symptoms, and a flu-like malaise; and increased PMN-elastase is correlated with concentration difficulties, failing memory and a subjective experience of infection."


    "The findings show that ME/CFS is characterized by low-grade inflammation and activation of CMI. The results suggest that characteristic symptoms of ME/CFS, such as fatigue, autonomic symptoms and a flu-like malaise, may be caused by inflammatory mediators, e.g. IL-1 and TNFα."

    See more here: http://www.ncbi.nlm.nih.gov/pubmed/21975140

    N-Acetylglucosamine Prevents IL-1β-Mediated Activation of Human Chondrocytes

    "Glucosamine represents one of the most commonly used drugs to treat osteoarthritis. However, mechanisms of its antiarthritic activities are still poorly understood. The present study identifies a novel mechanism of glucosamine-mediated anti-inflammatory activity. It is shown that both glucosamine and N-acetylglucosamine inhibit IL-1β- and TNF-α-induced NO production in normal human articular chondrocytes. The effect of the sugars on NO production is specific, since several other monosaccharides, including glucose, glucuronic acid, and N-acetylmannosamine, do not express this activity. Furthermore, N-acetylglucosamine polymers, including the dimer and the trimer, also do not affect NO production."

    "The observed suppression of IL-1β-induced NO production is associated with inhibition of inducible NO synthase mRNA and protein expression. In addition, N-acetylglucosamine also suppresses the production of IL-1β-induced cyclooxygenase-2 and IL-6. The constitutively expressed cyclooxygenase-1, however, was not affected by the sugar. N-acetylglucosamine-mediated inhibition of the IL-1β response of human chondrocytes was not associated with the decreased inhibition of the mitogen-activated protein kinases c-Jun N-terminal kinase, extracellular signal-related kinase, and p38, nor with activation of the transcription factor NF-κB. In conclusion, these results demonstrate that N-acetylglucosamine expresses a unique range of activities and identifies a novel mechanism for the inhibition of inflammatory processes"

    See more here:http://www.jimmunol.org/content/166/8/5155.full

    Last edited: Mar 10, 2015
  2. RadioFM

    RadioFM Active Member

    "The findings show that ME/CFS is characterized by low-grade inflammation and activation of CMI. "

    "Cell-mediated immunity is an immune response that does not involve antibodies, but rather involves the activation of phagocytes, antigen-specific cytotoxic T-lymphocytes, and the release of various cytokines in response to an antigen. Historically, the immune system was separated into two branches: humoral immunity, for which the protective function of immunization could be found in the humor (cell-free bodily fluid or serum) and cellular immunity, for which the protective function of immunization was associated with cells. CD4 cells or helper T cells provide protection against different pathogens. Cytotoxic T cells cause death by apoptosis without using cytokines, therefore in cell mediated immunity cytokines are not always present."

    "The innate immune system and the adaptive immune system each comprise both humoral and cell-mediated components."

    Cellular immunity protects the body by:

    1. "activating antigen-specific cytotoxic T-lymphocytes that are able to induce apoptosis in body cells displaying epitopes of foreign antigen on their surface, such as virus-infected cells, cells with intracellular bacteria, and cancer cells displaying tumor antigens;"
    2. "activating macrophages and natural killer cells, enabling them to destroy pathogens; and
    3. stimulating cells to secrete a variety of cytokines that influence the function of other cells involved in adaptive immune responses and innate immune responses."

    "Cell-mediated immunity is directed primarily at microbes that survive in phagocytes and microbes that infect non-phagocytic cells. It is most effective in removing virus-infected cells, but also participates in defending against fungi, protozoans, cancers, and intracellular bacteria. It also plays a major role in transplant rejection."

    See more here: http://en.wikipedia.org/wiki/Cell-mediated_immunity

    Cell Mediated Response

    Last edited: Mar 10, 2015
  3. RadioFM

    RadioFM Active Member

    N-Acetylglucosamine may be another key supplement to consider in mediating inflammation.

    Has glucosamine been studied in other autoimmune conditions?

    "In a small clinical study published in 2000 in Alimentary Pharmacology and Therapeutics, two thirds of a study group of children with treatment-resistant inflammatory bowel disease improved substantially after two years of treatment with n-acetylglucosamine. Studies to explore glucosamine’s potential for treating IBD, Crohn’s disease and ulcerative colitis are ongoing."

    "No significant side effects were reported in the studies, giving rise to hopes that glucosamine could be a safe, natural, inexpensive and effective way to treat autoimmune disorders."

    See more here: http://beforeitsnews.com/health/201...e-may-reverse-autoimmune-disease-2533190.html


    iherb.com N-AcetylGlucosamine
    http://www.iherb.com/search?kw=N-Acetyl Glucosamine#p=1
  4. RadioFM

    RadioFM Active Member

    Knockdown of interleukin-1α does not attenuate LPS-induced production of interleukin-1β in mouse macrophages?

    "Collectively, our findings do not support the previously suggested role of nuclear IL-1α in gene regulation of IL-1β. Rather, they suggest that IL-1α acts mainly as an alarmin that is sequestered in the nucleus following stimulation with TLR-4."

    See more : http://www.sciencedirect.com/science/article/pii/S1043466615000484

    Last edited: Mar 10, 2015
  5. jkennedy

    jkennedy Member

    Interesting about NAG. I had read about it on Phoenix Rising on a thread about supplements that reduce anxiety. The guy who started the thread said it also helps him with nasal congestion.

    I tried it a long time ago, but it made me feel really altered and weird. However, most people reporting on the thread I mentioned above have had positive experiences with it for anxiety. Some have mentioned relief from nasal congestion, too.

    I might try it again sometime. I could react differently now that my health is better than a couple of years ago.

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