title: 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.
abstract: BACKGROUND
  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.
  
  
  METHODS
  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.
  
  
  RESULTS
  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.
  
  
  CONCLUSIONS
  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.
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
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000097:blood; D015673:Fatigue Syndrome, Chronic / Q000097:blood / Q000276:immunology* / Q000503:physiopathology; D005260:Female; D006801:Humans; D007111:Immunity, Cellular / Q000276:immunology*; D007249:Inflammation / Q000276:immunology; D007375:Interleukin-1 / Q000097:blood / Q000276:immunology; D019272:Leukocyte Elastase / Q000097:blood / Q000276:immunology; D008297:Male; D008875:Middle Aged; D009113:Muramidase / Q000097:blood / Q000276:immunology; D019798:Neopterin / Q000097:blood / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000097:blood / Q000276:immunology
chemical_list: D015415:Biomarkers; D007375:Interleukin-1; D014409:Tumor Necrosis Factor-alpha; D019798:Neopterin; D009113:Muramidase; D019272:Leukocyte Elastase