Firestormm
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Received: July 27, 2011
Accepted after revision: January 20, 2012
Published online: July 20, 2012
Published in: Karger: Psychotherapy and Psychosomatics: http://content.karger.com/produktedb/produkte.asp?doi=336803
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
Michael Maes, Frank N.M. Twisk, Karl Ringel
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.
Copyright © 2012 S. Karger AG, Basel
Accepted after revision: January 20, 2012
Published online: July 20, 2012
Published in: Karger: Psychotherapy and Psychosomatics: http://content.karger.com/produktedb/produkte.asp?doi=336803
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
Michael Maes, Frank N.M. Twisk, Karl Ringel
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.
Copyright © 2012 S. Karger AG, Basel