Abstract
Three types of tachykinin receptors, namely NK1, NK2and NK3, are known to preferentially interact with substance P (SP), neurokinin A (NKA) and neurokinin B (NKB), respectively. We previously demonstrated that NK1and NK2receptors are present on human monocytes, SP and NKA inducing superoxide anion production and tumor necrosis factor- alpha (TNF-α) mRNA expression. NK2receptor stimulation also triggered an enhanced respiratory burst in monocytes isolated from rheumatoid arthritis (RA) patients. This study was aimed to evaluate the in vitro and ex-vivo effects of cyclosporin A (CsA) on tachykinins-evoked TNF-α release from monocytes of healthy donors and RA patients. CsA (100ng/ml) potently inhibited phorbol ester- and tachykinin-evoked TNF-α secretion. In RA patients treated with CsA (SandimmunRNeoralR) 2.5mg/kg/die, a significant time-dependent reduction in TNF-α secretion from monocytes was measured. This may contribute to the CsA therapeutic activity in RA.
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