Concentrations of IL-6 and sTNFR1 were measured using an enzyme-linked immunosorbent assay (ELISA), according to the manufacturer's specifications (Quantikine High Sensitivity Human for IL-6 and Quantikine Human sTNF RI/TNFRSF1A Immunoassay for sTNFR1; R&D Systems, USA).
The sTNFR1 levels increased after M30 exercise (P=0.
The delta sTNFR1 after M30 increased in relation to L30 and L45 (P=0.
This was evidenced by increased sTNFR1 and MDA levels after M30 exercise.
Studies in different populations (23-26) have reported an anti-inflammatory response immediately after a single exercise session, with an increase in plasma IL-6 and sTNFR1 levels, including in CHF patients.
Although with the results of the present study we cannot establish a cause-and-effect relationship between oxidative stress and inflammation, we hypothesized that the observed increase in MDA and sTNFR1 levels immediately after M30 exercise could be mediated by the production of the superoxide anion and hydrogen peroxide free radicals, stimulating the release of TNF-[alpha] and promoting lipid peroxidation (9).
The present results demonstrated increased levels of sTNFR2 in serum of patients with TR in comparison with controls, but no differences in TNF-[alpha] and sTNFR1 levels were found.
As previous studies have suggested that sTNFR1 and sTNFR2 are the natural homeostatic regulators of the TNF-[alpha] (11,29) and seem to be reliable markers of TNF-[alpha] activity (8,12,13), the present finding of elevated sTNFR2 suggests the involvement of TNF-[alpha] in human TR.
The distinct behavior of sTNFR1 and sTNFR2 in TR is not unique and has been reported in other infectious diseases.
Concentrations of CXCL8, CXCL9 and sTNFR1 in plasma of patients with pulmonar tuberculosis undergoing treatment.