Increased tolerance to endotoxin by granulocyte-macrophage colony-stimulating factor-deficient mice
- Author(s)
- Basu, S; Dunn, AR; Marino, MW; Savoia, H; Hodgson, G; Lieschke, GJ; Cebon, J;
- 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
- Terms of Use/Rights Notice
- Refer to copyright notice on published article.
Creation Date: 1997-08-01 12:00:00