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

LH Faccioli, GEP Souza, FQ Cunha, S Poole… - Agents and actions, 1990 - Springer
LH Faccioli, GEP Souza, FQ Cunha, S Poole, SH Ferreira
Agents and actions, 1990Springer
The α and β forms of recombinant interleukin-1 (IL-1α and IL-1β) and of recombinant Tumor
Necrosis Factor (TNFα and TNFβ) induced dose-dependent neutrophil migration into rat
peritoneal cavities. Migration induced by both IL-1s showed a bell-shaped dose-response
curve and IL-1β was 3-fold more potent than IL-1α. 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 …
Abstract
The α and β forms of recombinant interleukin-1 (IL-1α and IL-1β) and of recombinant Tumor Necrosis Factor (TNFα and TNFβ) induced dose-dependent neutrophil migration into rat peritoneal cavities. Migration induced by both IL-1s showed a bell-shaped dose-response curve and IL-1β was 3-fold more potent than IL-1α. 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-1β 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-1α, IL-1β and TNFβ is not due to a direct effect on neutrophils, but occurs via the release of a chemotactic factors(s) from resident macrophages.
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