Cytokine network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome

• Published in: Molecular psychiatry 2016-02, Vol.21 (2), p.261-269
• Main Authors: Hornig, M, Gottschalk, G, Peterson, D L, Knox, K K, Schultz, A F, Eddy, M L, Che, X, Lipkin, W I
• Format: Article
• Language: English
• Subjects: 692/53/2421; 82; Adult; Age; Autoimmunity; Behavioral Sciences; Biological Psychology; Care and treatment; Case-Control Studies; Central nervous system; Cerebrospinal fluid; Chemokine CCL11 - immunology; Chemokine CCL11 - metabolism; Chemokines; Chronic fatigue syndrome; Cognitive ability; Colonies; Colony-stimulating factor; Cytokines; Cytokines - analysis; Cytokines - cerebrospinal fluid; Cytokines - immunology; Dengue fever; Diagnosis; Encephalitis; Encephalomyelitis; Eotaxin; Fatigue; Fatigue Syndrome, Chronic - immunology; Fatigue Syndrome, Chronic - metabolism; Female; Health aspects; Herpes viruses; Humans; Immune response; Immunoassay; Infections; Interleukin 1; Interleukin 1 receptor antagonist; Interleukin-17; Interleukin-1beta; Internal medicine; Leukocytes (eosinophilic); Macrophage colony-stimulating factor; Male; Medicine; Medicine & Public Health; Middle Aged; Multiple sclerosis; Multiple Sclerosis - cerebrospinal fluid; Multiple Sclerosis - immunology; Multiple Sclerosis - metabolism; Nervous system; Neurosciences; original-article; Pharmacotherapy; Proteins; Psychiatry; Public health; West Nile virus
• ISSN: 1359-4184; 1476-5578
• DOI: 10.1038/mp.2015.29

Myalgic encephalomyelitis/chronic fatigue syndrome is an unexplained debilitating disorder that is frequently associated with cognitive and motor dysfunction. We analyzed cerebrospinal fluid from 32 cases, 40 subjects with multiple sclerosis and 19 normal subjects frequency-matched for age and sex using a 51-plex cytokine assay. Group-specific differences were found for the majority of analytes with an increase in cases of CCL11 (eotaxin), a chemokine involved in eosinophil recruitment. Network analysis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating factor 1, colony-stimulating factor 2 and interleukin 17F, without effects on interleukin 1α or interleukin 1β, suggesting a disturbance in interleukin 1 signaling. Our results indicate a markedly disturbed immune signature in the cerebrospinal fluid of cases that is consistent with immune activation in the central nervous system, and a shift toward an allergic or T helper type-2 pattern associated with autoimmunity.