Lipopolysaccharide (LPS)-induced cell death of C3H mouse peritoneal macrophages in the presence of cycloheximide: different susceptibilities of C3H/HeN and C3H/HeJ mice macrophages

Abstract

Lipopolysaccharide (LPS) induced cytotoxicity toward mouse peritoneal macrophages from C3H/HeN mice but not C3H/HeJ mice in vitro in the presence of cycloheximide (CHX). More than 1 ng/ml LPS induced a significant time-dependent release of a cytoplasmic enzyme, lactate dehydrogenase (LDH), while even 1000 ng/ml LPS failed to induce it in LPS-non-responsive C3H/HeJ mouse macrophages. Although similar LPS-induced cytotoxicity was observed in a murine macrophage-like cell line, J774.1, but not in an LPS-resistant mutant of J774.1, the LPS1916 cell line, these results suggest that the induction of this cytotoxicity is linked to the LPS-sensitivity of mouse macrophages. A recombinant TNF-α (rTNF-α) at 100 ng/ml augmented LDH release from both C3H/HeN and C3H/HeJ macrophages treated with LPS and CHX, while rTNF-α alone or in combination with LPS or CHX failed to induce LDH release. These results suggest that this cytotoxicity might be partially regulated by high concentrations of exogenous TNF-α in both C3H/HeN and C3H/HeJ macrophages, implying a possibility of paracrine regulation of TNF-α in mice toward LPS-treated macrophages under impaired protein synthesis.

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