Role of endogenous tumor necrosis factor alpha and interleukin 1 for experimental tumor growth and the development of cancer cachexia.

摘要: The aim of this study was to evaluate what extent tumor necrosis factor α (TNF-α) and interleukin 1 may explain the development experimental cancer cachexia. For purpose, C57BL/6J mice bearing a transplantable low differentiated rapidly growing were passively immunized every other day with rabbit or rat neutralizing immunoglobulins against either TNF-α (anti-TNF) an receptor (anti-IL-lr). Anti-IL-1r in itself had no agonistic effect type I, T-cell/fibroblast IL-receptor. Tumor-bearing receiving preimmune antiserum nonimmune hybridoma IgG served as controls. Anti-TNF anti-IL-1r inhibited growth significantly, measured by lower wet dry weight at end 11 days treatment ( P < 0.05). acute phase response tumor-bearing animals, increase liver weight, hepatic RNA content, increases plasma concentrations circulating IL-6, serum amyloid P, transferrin, complement (C3), decrease albumin, unaffected specific treatments. Food intake, which declined significantly pre/nonimmune injected controls, improved animals IL-1r. Whole body lipid content showed trend improvement specifically 0.07). effects on whole fat-free insignificant, although numerically higher animals. combination anti-TNF additive compared single suggesting that two antibody treatments acted through common mechanism. Cultured cells, established from tumors, sensitive anti-IL-1r, both reduced vitro . This inhibitory could part be reversed addition recombinant IL-1α TNFα. We conclude TNF IL-1 are involved thus progression It seems if role promote rather than restrict present model. In sense act factors.