A new 2015 study, published in the Mediators of Inflammation journal suggests a deficiency of interleukin (IL)-10 in chronic fatigue syndrome (CFS).
Chronic fatigue syndrome/myalgic encephalomyelitis, an illness characterized by unexplained fatigue lasting 6 months or more, is often linked to dysfunctional neuroendocrine and immune responses, including abnormal production of several cytokines (NG Klimas & A O’Brien Koneru, 2007). The term CFS was introduced in 1988 but an umbrella term – neuroendocrine-immune dysfunction syndrome (CNDS) is also often used (LA Jason et al., 2003).
The ‘immune hormone’ IL-10 is a major anti-inflammatory cytokine in periphery and the central nervous system (CNS). IL-10 downregulates the pro-inflammatory immune responses related to the T helper (Th1) cell axis, and, in general, the production of most of the pro-inflammatory cytokines. This includes a suppression of cytokine production and the expression of cytokine receptors in brain’s microglia cells (M Sawada et al., 1999).
In the Mediators of Inflammation study, D. Peterson and colleagues from the Simmaron Research, NV, USA and the Griffith University, Parklands, Australia collected cerebrospinal fluid (CSF) samples from CFS patients at the time of diagnosis, and cytokines were analyzed via the Bio-Plex Pro Human Cytokine 27-plex Assay (Bio-Rad).
The authors report that of the 27 cytokines examined; only IL-10 was significantly decreased in the CFS group, as compared to healthy control individuals. Further studies may be required to identify and/or confirm whether the putative IL-10 deficiency may contribute to increased pro-inflammatory activities in CFS.