Diagnostic value of IL-17 in neurointoxication with mercury

It is known that sufficient changes are observed in cellular and humoral links of immune system upon chronic exposure vapors of metallic mercury. In previous studies, upon development and in the course of the chronic mercury intoxication (CMI) we revealed pronounced regular changes of inflammatory mediators (IL-1, IL-2, IL-4, IL-6, IL-8, IL-10, TNFα), and showed an important role of autoimmune reactions affecting nervous tissue proteins. Over last 20 years, an increased interest was shown for interleukin 17 (IL-17) and its role in a number of inflammatory and autoimmune diseases. However, there is no data on its role in neurointoxication with mercury. Considering that IL-17 has proinflammatory activity and stimulates production of the individual cytokines, the goal of our work at the next stage of research, was to identify quantitative changes of serum IL-17 in patients with mercury neurointoxication of various severity, aiming to substantiate additional criteria for early and effective diagnosis of the disease.The study was performed in males chronically exposed to metallic mercury vapors with early signs of neurointoxication (n = 37), individuals diagnosed with CMI (n = 40), and “conditionally healthy” men (n = 34). Proper diagnosis confirmed by history of working contacts with a harmful industrial factor, and absence of comorbid pathologies served as inclusion criteria. Statistical processing of the results was carried out using the STATISTICA 6.0 application package (StatSoft, USA). The study has revealed a statistically significant increase in serum IL-17 concentrations, both in the patients with early signs of neurointoxication with metallic mercury vapors, and individuals with CMI, when compared with the comparison group, thus indicating its activation, and being consistent with results of several workers who showed an IL-17 increase in immunoinflammatory diseases. Correlation analysis has shown an association between IL-17 and inflammatory mediators, i.e., the patients with early signs of neurointoxication had an increased production of IL-17 accompanied by an increase in anti-inflammatory IL-10, whereas the CMI patients with an increase in IL-17 concentration showed a decrease in pro-inflammatory TNFα, thus confirming its role in immunopathogenesis of mercury neurointoxication. Further study of IL-17 involvement in the initiation and maintenance of chronic inflammation will not only contribute to better understanding of the disease origin, but also, most importantly, implication of novel, more effective treatments.