Evidence that endogenous interleukin-1 is involved in leukocyte migration in acute experimental inflammation in rats and mice

Abstract

As a putative mediator of inflammation interleukin-1 has been implicated in the recruitment of leukocytes during the early stages of the inflammatory reaction. In the present report we have investigated the release of endogenous IL-1 in the rat zymosan pleurisy and in the mouse zymosan peritonitis. In both cases the release of the cytokine was maximal 4 hours after zymosan injection and appeared to be time-related to neutrophil migration into the inflammatory site. The effect ofin vivo treatment with dexamethasone in rat pleurisy and with polyclonal anti-murine IL-1β antibody in mouse peritonitis was also assessed. The steroid reduced both cell migration and the release of IL-1-like activity as well as the formation of exudate and the release of eicosanoids. The anti-IL-1β serum inhibited selectively the number of neutrophil that migrated to the inflamed site (∼40%) and the IL-1 activity recovered in (∼70%) the exudate.In vitro incubation of the inflammatory exudate with polyclonal anti-murine IL-1α or anti-murine IL-1β sera allowed the identification of the IL-1 species present. In the rat pleurisy IL-1 biological activity was mainly due to the α species, whereas IL-1β was the only species apparently present in the mouse peritoneal exudate.