Activation and Apoptosis of Murine Peritoneal Macrophages by Acute Cold Stress

Authors: Kizkai T.1; Suzuki K.1; Hitomi Y.1; Iwabuchi K.3; Onoé K.3; Ishida H.2; Izawa T.4; Ji L.L.5; Ohno H.1

Source: Biochemical and Biophysical Research Communications, Volume 283, Number 3, May 2001 , pp. 700-706(7)

Publisher: Academic Press

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Abstract:

Effects of acute cold stress (5°C for 24 h) on the functions of peritoneal macrophages and the mechanisms for controlling host homeostasis were investigated in mice. Phagocytic activity and expression of the cell surface adhesion molecule CD11b/CD18 were markedly increased in peritoneal exudate cells by acute cold stress. These alterations were attributable to an increased number and phenotypical changes of adherent cells from acute cold-stressed mice. On the other hand, a lipopolysaccharide-induced activity of src-family tyrosine kinase Fgr, an expression of interleukin-1beta (IL-1 beta) mRNA, and a bioactivity of IL-1 in the culture supernatants of adherent cells from acute cold-stressed mice were markedly lower than those from control mice. A time course study revealed that the number of adherent cells in peritoneal exudate cells was markedly increased in mice exposed to cold for 24 h but returned to normal numbers when mice were exposed to cold for 72 h. DNA fragmentation and Annexin-V+ cells were observed in peritoneal exudate cells from acute-cold stressed mice. Thus, cold stress activated macrophages but these macrophages were destined to be eliminated by apoptosis. Copyright 2001 Academic Press.

Keywords: phagocytosis; IL-1; LPS; DNA fragmentation; apoptosis; Fgr

Language: English

Document Type: Research article

Affiliations: 1: Department of Molecular Predictive Medicine and Sport Science 2: Department of Molecular Predictive Medicine and Sport Science, Third Department of Medicine, Kyorin University, School of Medicine, Tokyo, Mitaka, 181-8611, Japan 3: Institute for Genetic Medicine, Hokkaido University, Hokkaido, Sapporo, 060-0815, Japan 4: Graduate School of Science, Tokyo Metropolitan University, Tokyo, Hachioji, 192-0397, Japan 5: Department of Physiology and Pharmacology, Karoliska Institute, Stockholm, Lidingovagen, 11486, Sweden

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