“…The clinical manifestations of SE intoxication are associated primarily with the large-scale release of pro-inflammatory cytokines, particularly interleukin 2 (IL-2) and tumor necrosis factor a (TNFa) (Marrack and Kappler, 1990;Johnson et al, 1991;Miethke et al, 1992), as a result of the massive proliferation of T lymphocytes. However, fipram SEs exert a direct effect on the target organs, particularly the kidney, thereby contributing to the dysregulation of vascular tone, which results in severe hypotension associated with SE-induced toxic shock (Chatterjee and Jett, 1992;Chatterjee etal., 1995;Khullar and Chatterjee, 1995;Ionin et al, 2000).…”