Recombinant interleukin-1 and tumor necrosis factor induce neutrophil migration "in vivo" by indirect mechanisms

• Published in: Agents and actions Vol. 30; no. 3-4; p. 344
• Main Authors: Faccioli, L H, Souza, G E, Cunha, F Q, Poole, S, Ferreira, S H
• Format: Journal Article
• Language: English
• Published: Switzerland 01.06.1990
• Subjects: Animals; Cell Migration Inhibition; Chemotactic Factors - physiology; Chemotaxis, Leukocyte - physiology; Interleukin-1 - physiology; Interleukin-8; Lipopolysaccharides - physiology; Macrophages - metabolism; Male; Neutrophils - physiology; Rats; Rats, Inbred Strains; Recombinant Proteins - pharmacology; Tumor Necrosis Factor-alpha - physiology
• ISSN: 0065-4299
• DOI: 10.1007/bf01966298

The alpha and beta forms of recombinant interleukin-1 (IL-1 alpha and IL-1 beta) and of recombinant Tumor Necrosis Factor (TNF alpha and TNF beta) induced dose-dependent neutrophil migration into rat peritoneal cavities. Migration induced by both IL-1s showed a bell-shaped dose-response curve and IL-1 beta was 3-fold more potent than IL-1 alpha. Pretreatment of the animals with dexamethasone or depletion of the peritoneal macrophage population, abolished the neutrophil migration induced by the four cytokines. "In vitro" stimulation of macrophage monolayers with IL-1 beta and the TNFs released a factor into the supernatant which, unlike these cytokines, induced neutrophil migration in dexamethasone pretreated animals. These results suggest that the neutrophil migration induced by IL-1 alpha, IL-1 beta, TNF alpha and TNF beta is not due to a direct effect on neutrophils, but occurs via the release of a chemotactic factor(s) from resident macrophages.