Lipopolysaccharides

From MEpedia, a crowd-sourced encyclopedia of ME and CFS science and history

Lipopolysaccharides (LPS) also known as lipoglycans and endotoxins are large molecules found on the outer membrane of gram-negative bacteria. They provoke a strong innate immune response. LPS is an exogenous pyrogen.

One study found higher levels of serum IgA and IgM against LPS in chronic fatigue syndrome patients, indicating bacterial translocation from the intestine into the bloodstream. [1]. Serum IgA was significantly correlated to the severity of illness.

A study of 128 ME/CFS patients found significantly increased IgA response to lipopolysaccharides (LPS) from the cell walls of commensal bacteria. Increased IgA response was associated with increased serum IL-1, TNFα, neopterin and elastase. The study concluded that increased translocation of commensal bacteria may be responsible for the disease activity in some ME/CFS patients.[2]

A study of 48 ME/CFS patients and 39 controls in 2016 found elevated levels of LPS in patients.[3]

Some LPS molecules have been implicated in autoimmune disease including multiple sclerosis[4][5] and Guillain-Barré syndrome[6].

A study in 2000 found that direct electrical stimulation of the vagus nerve in rats decreased the inflammatory response to LPS.[7]

See also[edit | edit source]

References[edit | edit source]

  1. ↑ Maes, Michael; Mihaylova, Ivana; Leunis, Jean-Claude (April 1, 2007). "Increased serum IgA and IgM against LPS of enterobacteria in chronic fatigue syndrome (CFS): Indication for the involvement of gram-negative enterobacteria in the etiology of CFS and for the presence of an increased gut–intestinal permeability". Journal of Affective Disorders. 99 (1): 237–240. doi:10.1016/j.jad.2006.08.021. ISSN 0165-0327.
  2. ↑ Increased IgA responses to the LPS of commensal bacteria is associated with inflammation and activation of cell-mediated immunity in chronic fatigue syndrome, Maes M1, Twisk FN, Kubera M, Ringel K, Leunis JC, Geffard M., J Affect Disord. 2012 Feb;136(3):909-17. doi: 10.1016/j.jad.2011.09.010. Epub 2011 Oct 2.
  3. ↑ Giloteaux, Ludovic; Goodrich, Julia K.; Walters, William A.; Levine, Susan M.; Ley, Ruth E.; Hanson, Maureen R. (June 23, 2016). "Reduced diversity and altered composition of the gut microbiome in individuals with myalgic encephalomyelitis/chronic fatigue syndrome". Microbiome. 4: 30. doi:10.1186/s40168-016-0171-4. ISSN 2049-2618. PMC 4918027. PMID 27338587.
  4. ↑ Chastain, Emily M.L.; Miller, Stephen D. (January 2012). "Molecular mimicry as an inducing trigger for CNS autoimmune demyelinating disease". Immunological Reviews. 245 (1): 227–238. doi:10.1111/j.1600-065X.2011.01076.x. ISSN 1600-065X. PMC 3586283. PMID 22168423.
  5. ↑ Moran, A.P.; Prendergast, M.M.; Appelmelk, B.J. (December 1, 1996). "Molecular mimicry of host structures by bacterial lipopolysaccharides and its contribution to disease". FEMS immunology and medical microbiology. 16 (2): 105–115. doi:10.1111/j.1574-695X.1996.tb00127.x. ISSN 0928-8244. PMID 8988391.
  6. ↑ Moran, A.P.; Prendergast, M.M.; Appelmelk, B.J. (December 1, 1996). "Molecular mimicry of host structures by bacterial lipopolysaccharides and its contribution to disease". FEMS immunology and medical microbiology. 16 (2): 105–115. doi:10.1111/j.1574-695X.1996.tb00127.x. ISSN 0928-8244. PMID 8988391.
  7. ↑ Borovikova, Lyudmila V.; Ivanova, Svetlana; Zhang, Minghuang; Yang, Huan; Botchkina, Galina I.; Watkins, Linda R.; Wang, Haichao; Abumrad, Naji; Eaton, John W.; Tracey, Kevin J. (May 2000). "Vagus nerve stimulation attenuates the systemic inflammatory response to endotoxin". Nature. 405 (6785): 458–462. doi:10.1038/35013070. ISSN 1476-4687.
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