THU0097 Neurogenic Inflammation in Rheumatoid Arthritis : Possible Role of Neuropeptides on Synovial Vanilloid Receptors

Background Neurogenic inflammation is caused by neuropeptides, like substance P (SP) and calcitonin gene related peptide (CGRP), which are released by peripheral neurons and induce inflammatory signals. SP and CGRP act through several molecular mechanisms including activation of transient receptor potential vanilloid (TRPV) cation channels, particularly TRPV1. SP and CGRP have been found increased in synovial fluid from rheumatoid arthritis (RA) patients and may induce the production of interleukin in RA synoviocytes 1. TRPV cation channels are expressed in various non-neuronal cell types including human synoviocytes 2. Objectives To investigate whether neuropeptides can increase IL-8 production of synoviocytes as pivotal cytokine involved in joint inflammation. To investigate whether SP and CGRP are able to modulate expression of TRPV1 in RA and healthy synoviocytes. Methods RA and healthy synoviocytes were cultured and incubated at 6 hours (SP 10-7M, CGRP10-8M, baseline) and 24 hours (SP 10-7M, CGRP10-8M, SP 10-7M+CAP 10-6M, CGRP 10-8M+CAP 10-6M, baseline). Supernatant of cells incubated 24 hours were assayed by specific ELISA IL-8 Kit. Cells incubated for 6 hours were collected and levels of mRNA of TRPV1 were assayed by Real-Time PCR. Supernatant IL-8 and TRPV1 mRNA are expressed as mean ± standard deviations (SD) and compared by Mann-Whitney Test and t-Student test. The differences are considered significant for p