Inflammatory and cell-mediated immune biomarkers in myalgic encephalomyelitis/chronic fatigue syndrome and depression: inflammatory markers are higher in myalgic encephalomyelitis/chronic fatigue syndrome than in depression

Abstract

BACKGROUND: Depression is an inflammatory disorder while many authors declare myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) to be a functional  disorder. The aim of the present study is to compare inflammatory and  cell-mediated immune (CMI) responses between depression and ME/CFS. METHODS: We  measured two proinflammatory cytokines (PICs) in plasma, interleukin-1 (IL-1) and  tumor necrosis factor-α (TNF-α), with enzyme-linked immunosorbent assays, and  serum neopterin with a radioimmunoassay in controls, ME/CFS and depressive  patients. RESULTS: Plasma PICs were significantly higher in ME/CFS than in  depression and higher in both patient groups than in controls. Increased PIC  levels in depression were attributable to the presence of fatigue and  physio-somatic symptoms. Serum neopterin did not differ significantly between  depression and ME/CFS but was higher in both patient groups than in controls. The  significant positive correlations between neopterin and either IL-1 or TNF-α were  significantly greater in depression than in ME/CFS. CONCLUSIONS: Since PICs cause  depression-like behaviors and fatigue/malaise, we suggest that inflammation may  play a role in the pathophysiology of ME/CFS and depression. Increased neopterin  also seems to contribute to the pathophysiology of both disorders. This study has  detected a shared 'pathway phenotype', i.e. disorders in inflammatory and CMI  pathways, which underpins both ME/CFS and depression and, therefore, may explain  the co-occurrence of both disorders. ME/CFS and depression are discriminated from  each other by increased PICs in ME/CFS and differences in the immune cell  communication networks.