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.