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Giovanni Antioco Putzu,

Giovanni Antioco Putzu,

Hospital de Santa Maria, Portugal

Title: Tumor Necrosis Factor alpha (TNF-alpha) and pro-inflammatory cytokines in vaculitis of Peripheral Nervous System.

Biography

Biography: Giovanni Antioco Putzu,

Abstract

We demonstrated, by the means of double immunochemistry technique, that TNF-alpha was localized in both axons and Schwann Cells, leading to demyelination and axonal in the peripheral nerve of patients with Guillain-Barré Syndrome (GBS, Putzu G.A. et al, J. Neurol. Sci, 2000). The pivotal role of pro-inflammatory cytokines such as IL-1Beta in GBS was also investigated. We present an original immunochemistry study with a panel of antibodies directed against TNF-alpha, INF-gamma, IL-1Beta, CD68, CD11, CD3 and C5b9 in the peripheral nerve of seventy-five patients affected by vasculitis. Sixty patients (27 males and 23 females, mean age 63 years) were classified as systemic vasculitic neuropathy (SVN) where as 15 patients (7 males and 8 females, mean age 52 years) had non systemic vasculitic neuropathy (NSVN). Results suggested a prevalent Th1 immune response in both SVN e NSVN. The presence of great amounts of TNF alpha and IL-1Beta into the vasculature determines a pro-coagulant effect with thrombosis of the vasa nervorum and hypoxia of the nervous fascicules. TNF-alpha was localized in axons as well, suggesting that it may be responsible for an axonal degeneration per se. Peripheral nerves of SNV e NSVN were immunoreactive to INF-gamma antibodies. This finding indirectly confirms the presence in the vasculature of IL-28A, a powerful pro-inflammatory cytokines. CD11, an antibody reacting with leucocytes and ICAM (Intercellular Adhesion Molecule) was also detected in the peripheral nerve of SVN and NSVN. Immunoreactivity to CD68 (macrophage antigen) and C5b9 (activated complement fraction) were also easily detected. In conclusion, immune response in SVN and NSVN is of Th 1 type (cellular). The role of TNF-alpha and cytokines is crucial in vascular thrombosis. Axonal degeneration may be the consequence of both hypoxia and direct toxic effect of TNF-alpha on axons. Moreover, pattern of immune response is not specific in SVN and NSVN