Abstract
Septic arthritis is an inflammatory joint disease caused by S. aureus. Hematogenous entry of the bacteria to the joint space secretespro-inflammatory cytokines TGF-β and IL-6, which alter the Th17/Treg switch. Inhibition of TGF-β and IL-6 to modulate Th17/Treghomeostasis and RANKL/OPG interaction are not done so far in septic arthritis. Role of lymphocyte-derived TGF-β, IL-10, IL-21 alongwith OPN, OPG, cellular H2O2, SOD and catalase activities, and the expressions of RANKL and MMP2 were studied in total lymphocytesof blood, spleen and synovial tissues of Swiss albino mice treated with antibody against TGF-β along with IL-6 Ab after induction ofseptic arthritis. Simultaneous neutralization of TGF-β along with IL-6 is effective in shifting the Th17 cell into Treg cell of the arthriticmice and modulates RANKL and MMP2 expression that leads to the down-regulation of osteoclastic activity and reduces the production of OPN. Additionally, such treatment reduces oxidative stress via enhancing the activities SOD and catalase enzymes in lymphocytes. So, simultaneous neutralization of TGF-β and IL-6 reduces S. aureus infection-associated inflammatory joint damage by increasing Treg numbers and decreasing the number of pro-inflammatory Th17 cells.
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