title: Increased IgA responses to the LPS of commensal bacteria is associated with inflammation and activation of cell-mediated immunity in chronic fatigue syndrome.
abstract: BACKGROUND
  Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is accompanied by a) systemic IgA/IgM responses against the lipopolysaccharides (LPS) of commensal bacteria; b) inflammation, e.g. increased plasma interleukin-(IL)1 and tumor necrosis factor (TNF)α; and c) activation of cell-mediated immunity (CMI), as demonstrated by increased neopterin.
  
  
  METHODS
  To study the relationships between the IgA/IgM responses to the LPS of microbiota, inflammation, CMI and the symptoms of ME/CFS we measured the IgA/IgM responses to the LPS of 6 different enterobacteria, serum IL-1, TNFα, neopterin, and elastase in 128 patients with ME/CFS and chronic fatigue (CF). Severity of symptoms was assessed by the Fibromyalgia and Chronic Fatigue Syndrome (FF) Rating Scale.
  
  
  RESULTS
  Serum IL-1, TNFα, neopterin and elastase are significantly higher in patients with ME/CFS than in CF patients. There are significant and positive associations between the IgA responses to LPS and serum IL-1, TNFα, neopterin and elastase. Patients with an abnormally high IgA response show increased serum IL-1, TNFα and neopterin levels, and higher ratings on irritable bowel syndrome (IBS) than subjects with a normal IgA response. Serum IL-1, TNFα and neopterin are significantly related to fatigue, a flu-like malaise, autonomic symptoms, neurocognitive disorders, sadness and irritability.
  
  
  CONCLUSIONS
  The findings show that increased IgA responses to commensal bacteria in ME/CFS are associated with inflammation and CMI activation, which are associated with symptom severity. It is concluded that increased translocation of commensal bacteria may be responsible for the disease activity in some ME/CFS patients.
authors.affiliation: Maes Clinics @ TRIA, Bangkok, Thailand. dr.michaelmaes@hotmail.com
authors.forename: Michael
authors.initials: M
authors.lastname: Maes
authors.forename: Frank N M
authors.initials: FN
authors.lastname: Twisk
authors.forename: Marta
authors.initials: M
authors.lastname: Kubera
authors.forename: Karl
authors.initials: K
authors.lastname: Ringel
authors.forename: Jean-Claude
authors.initials: JC
authors.lastname: Leunis
authors.forename: Michel
authors.initials: M
authors.lastname: Geffard
mesh_terms: D000293:Adolescent; D000328:Adult; D018988:Bacterial Translocation / Q000276:immunology; D002908:Chronic Disease; D004755:Enterobacteriaceae / Q000276:immunology* / Q000502:physiology; D005221:Fatigue / Q000276:immunology; D015673:Fatigue Syndrome, Chronic / Q000276:immunology*; D005260:Female; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology*; D007070:Immunoglobulin A / Q000276:immunology*; D007075:Immunoglobulin M / Q000276:immunology*; D007249:Inflammation / Q000276:immunology; D007375:Interleukin-1 / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D019798:Neopterin / Q000276:immunology; D010196:Pancreatic Elastase / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D007070:Immunoglobulin A; D007075:Immunoglobulin M; D007375:Interleukin-1; D008070:Lipopolysaccharides; D014409:Tumor Necrosis Factor-alpha; D019798:Neopterin; D010196:Pancreatic Elastase