Murine macrophages and pancreatic beta cells. Chemotactic properties of insulin and beta-cytostatic action of interleukin 1.

Abstract

This study has used in vitro techniques to investigate the potential interactions between mouse pancreatic islet cells and syngeneic macrophages (M phi). Islets strongly stimulated M phi migration from agarose microdroplets; insulin was the only one of four islet cell hormones tested that was effective individually. Chronic exposure of islet monolayers to recombinant mouse IL-1, an M phi secretory product, was not cytolytic, but inhibited insulin secretion, reduced intracellular insulin content, and produced beta cell-specific degranulation. These effects were unique to IL-1; another monokine, tumor necrosis factor, as well as the lymphokine IL-2, and lymphotoxin were all without effect on insulin secretion or monolayer viability at the concentrations tested. The potential pathological consequences of the chemoattractive action of insulin on M phi, and the inhibitory effect of IL-1 on insulin secretion, are discussed.