Increased tolerance to endotoxin by granulocyte-macrophage colony-stimulating factor-deficient mice
Details
Publication Year 1997-08-01, Volume 159, Issue #3, Page 1412-1417
Journal Title
JOURNAL OF IMMUNOLOGY
Publication Type
Journal Article
Abstract
The contribution of granulocyte-macrophage CSF (GM-CSF) to endotoxin-mediated septic shock has been assessed by treating GM-CSF-deficient mice with LPS. Hypothermia and loss in body weight were markedly attenuated in LPS-treated GM-CSF-deficient mice compared with similarly treated control mice; moreover, the levels of circulating IFN-gamma, IL-1 alpha, and IL-6 were lower in LPS-treated GM-CSF-deficient mice than LPS-treated control mice, intriguingly, the peak levels of TNF-alpha e to LPS treatment were the same in the serum of GM-CSF-deficient mice and control mice, although in GM-CSF-deficient mice, TNF-alpha persisted longer, Activation of macrophages by LPS, resulting in expression of cytokines including TNF-alpha and IL-1, is thought to underlie endotoxin-mediated effects, Accordingly, the response of peritoneal macrophages from CM-CSF-deficient mice to LPS was studied in vitro. LPS-stimulated peritoneal macrophages from GM-CSF-deficient mice produced significantly less IL-alpha and nitric oxide than macrophages from wild-type mice, although there was no difference in TNF-alpha production, Collectively, these observations indicate that GM-CSF contributes to cytokine production in LPS-mediated septic shock, and that the attenuated production of these secondary cytokines (IFN-gamma, IL-1 alpha, and IL-6) may contribute to the endotoxin-resistant phenotype of GM-CSF-deficient mice.
Publisher
AMER ASSOC IMMUNOLOGISTS
Keywords
TUMOR-NECROSIS-FACTOR; NITRIC-OXIDE SYNTHASE; FACTOR-ALPHA; INTERFERON-GAMMA; SEPTIC SHOCK; IFN-GAMMA; INTERLEUKIN-6; EXPRESSION; RESISTANT; TOXICITY
Rights Notice
Refer to copyright notice on published article.


Creation Date: 1997-08-01 12:00:00
Last Modified: 0001-01-01 12:00:00
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