Weight loss in obese mice persistently infected with lymphocytic choriomeningitis virus is not associated with elevated tumor necrosis factor/cachectin activity in peritoneal macrophages.
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Journal: 1988/September - American Journal of Pathology
ISSN: 0002-9440
PUBMED: 3414785
Abstract:
C57BL/6 ob/ob (C57 ob/ob) mice infected persistently with lymphocytic choriomeningitis virus (LCMV) show cachexia as judged by a weight loss of greater than 20%. Virus persists in a subset of macrophages. Because a cachexic state occurs in several chronic debilitating diseases of humans, often accompanied by persistent microbial infections with macrophage/monocytic involvement and tumor necrosis factor (TNF) cachectin production, the role of TNF in the weightloss of ob/ob mice infected persistently with LCMV was investigated. TNF mRNA expression was not increased in peritoneal cells from such persistently-infected mice, nor did their serum levels of TNF rise above those in uninfected litter-mates. Furthermore, in vitro LCMV infection of adherent peritoneal cells from these C57 ob/ob mice did not enhance TNF mRNA or protein expression. Therefore, the cachexia-like weight loss observed in C57 ob/ob mice during a persistent LCMV infection is apparently not associated with a measurable increase in TNF.
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Am J Pathol 132(3): 586-592
PMID: 3414785

Weight loss in obese mice persistently infected with lymphocytic choriomeningitis virus is not associated with elevated tumor necrosis factor/cachectin activity in peritoneal macrophages.

Abstract

C57BL/6 ob/ob (C57 ob/ob) mice infected persistently with lymphocytic choriomeningitis virus (LCMV) show cachexia as judged by a weight loss of greater than 20%. Virus persists in a subset of macrophages. Because a cachexic state occurs in several chronic debilitating diseases of humans, often accompanied by persistent microbial infections with macrophage/monocytic involvement and tumor necrosis factor (TNF) cachectin production, the role of TNF in the weightloss of ob/ob mice infected persistently with LCMV was investigated. TNF mRNA expression was not increased in peritoneal cells from such persistently-infected mice, nor did their serum levels of TNF rise above those in uninfected litter-mates. Furthermore, in vitro LCMV infection of adherent peritoneal cells from these C57 ob/ob mice did not enhance TNF mRNA or protein expression. Therefore, the cachexia-like weight loss observed in C57 ob/ob mice during a persistent LCMV infection is apparently not associated with a measurable increase in TNF.

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Selected References

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Department of Immunology, Research Institute of Scripps Clinic, La Jolla, California 92037.
Department of Immunology, Research Institute of Scripps Clinic, La Jolla, California 92037.
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Abstract
C57BL/6 ob/ob (C57 ob/ob) mice infected persistently with lymphocytic choriomeningitis virus (LCMV) show cachexia as judged by a weight loss of greater than 20%. Virus persists in a subset of macrophages. Because a cachexic state occurs in several chronic debilitating diseases of humans, often accompanied by persistent microbial infections with macrophage/monocytic involvement and tumor necrosis factor (TNF) cachectin production, the role of TNF in the weightloss of ob/ob mice infected persistently with LCMV was investigated. TNF mRNA expression was not increased in peritoneal cells from such persistently-infected mice, nor did their serum levels of TNF rise above those in uninfected litter-mates. Furthermore, in vitro LCMV infection of adherent peritoneal cells from these C57 ob/ob mice did not enhance TNF mRNA or protein expression. Therefore, the cachexia-like weight loss observed in C57 ob/ob mice during a persistent LCMV infection is apparently not associated with a measurable increase in TNF.
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