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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

Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Tokyo, Japan

Fumio Amano

Department of Biochemistry and Cell Biology, National Institute of Infectious Diseases, Tokyo, Japan, fumigon{at}nih.go.jp

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- (rTNF-) at 100 ng/ml augmented LDH release from both C3H/HeN and C3H/HeJ macrophages treated with LPS and CHX, while rTNF- 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- in both C3H/HeN and C3H/HeJ macrophages, implying a possibility of paracrine regulation of TNF- in mice toward LPS-treated macrophages under impaired protein synthesis.

Journal of Endotoxin Research, Vol. 6, No. 1, 33-39 (2000)
DOI: 10.1177/09680519000060010501


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