Smoking is associated with several diseases and affects the immune system. Recently, published data demonstrate an involvement of Th17 and regulatory T cells (Tregs) in the pathogenesis of chronic pain and pain intensity. The role of these T cell subsets in smoking patients with chronic pain is nebulous so far. We therefore analyzed Th17 cells and Tregs in smokers and non-smokers suffering from chronic pain.
Analyses of T cell subsets, mRNA expression and T cell related cytokine profiles were done in 44 patients with chronic pain. 22 of these patients were smokers. Numbers of T cell subsets were quantified by flow cytometry. mRNA expression of the Th17 (RORγT) and Treg (FoxP3) specific transcription factors was determined by quantitative real-time PCR (qPCR), and levels of cytokines were measured by Human Cytokine Multiplex Immunoassay.
Compared to non-smokers, smokers showed significantly enhanced pain levels. On cellular basis, the number of pro-inflammatory Th17 cells (smokers: 2.±2.5 % vs. non-smokers: 0.5±0.4 %; p=0.04) was increased, whereas the amount of anti-inflammatory Tregs (smokers: 2.5±0.9 % vs. non-smokers: 3.1±1.1 %; p=0.02) was significantly decreased, resulting in an altered Th17/Treg ratio (Th17/Treg ratio: 0.9±1.0 in smokers vs. 0.2±0.1 in non-smokers; p<0.01). These findings were confirmed by qPCR. Analyses of cytokines revealed only marginal changes.
In chronic pain patients, smoking is associated with enhanced pain levels together with an imbalance of the Th17/Treg ratio. The shift of the Th17/Treg ratio towards inflammation may explain in part the increased pain intensity in these patients.
Registration Trial DRKS00005954