Abstract
Although the underlying metabolic cause of chronic fatigue syndrome (CFS) is unknown, specific defects have been proposed to exist in the skeletal muscle, the immune system and the neuroendo-crine system. Peripheral blood mononuclear cells from CFS patients and healthy controls were fractionated as adherent cells (monocyte-en-riched fraction) and non-adherent cells. We have investigated some activities of the former during in vitro culture. It was observed that the morphology (shape and size) of adherent cells from CFS patients, co-cultivated with homologous non-adherent cells, differed between CFS patients and healthy controls for 21 out of 25 (84%) paired samples (i.e., CFS patient and healthy control). Cytokine expression was examined for the adherent cell population collected from 14 CFS patients and 12 healthy controls. Unstimulated and LPS stimulated tumour necrosis factor-a (TNFa) expression was higher for monocytes from 7 out of 14 CFS patients. Unstimulated interleukin-β (IL-β) expression was higher for monocytes from 10 out of 14 CFS patients, whereas LPS-stimulated IL-β expression was higher for 8 out of 14 CFS patients. The proportional increase of IL-β and TNFa following LPS stimulation was lower for the majority of the CFS patients studied, suggesting that the monocytes from CFS patients were less responsive to LPS than the respective healthy controls. The basis for the abnormal in vitro monocyte maturation, the elevated unstimulated levels of IL-β expression and the abnormal response of the monocytes to LPS is unknown. The relevance of these findings to CFS pathogenesis is discussed.