Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0341503 (bacterial peritonitis)
 1,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mast cells are thought to contribute significantly to the pathology and mortality associated with anaphylaxis and other allergic disorders. However, studies using genetically mast cell-deficient WBB6F1-KitW/KitW-v and congenic wild-type (WBB6F1-+/+) mice indicate that mast cells can also promote health, by participating in natural immune responses to bacterial infection. We previously reported that repetitive administration of the c-kit ligand, stem cell factor (SCF), can increase mast cell numbers in normal mice in vivo. In vitro studies have indicated that SCF can also modulate mast cell effector function. We now report that treatment with SCF can significantly improve the survival of normal C57BL/6 mice in a model of acute bacterial peritonitis, cecal ligation and puncture (CLP). Experiments in mast cell-reconstituted WBB6F1-KitW/KitW-v mice indicate that this effect of SCF treatment reflects, at least in part, the actions of SCF on mast cells. Repetitive administration of SCF also can enhance survival in mice that genetically lack tumor necrosis factor (TNF)-alpha, demonstrating that the ability of SCF treatment to improve survival after CLP does not solely reflect effects of SCF on mast cell- dependent (or -independent) production of TNF-alpha. These findings identify c-kit and mast cells as potential therapeutic targets for enhancing innate immune responses.
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PMID:The c-kit ligand, stem cell factor, can enhance innate immunity through effects on mast cells. 985 20

Intraperitoneal injection of bone marrow-derived mast cells (BMMCs) has therapeutic efficacy against acute bacterial peritonitis. For this role, BMMCs need to settle down the mesentery from the peritoneal cavity. Interaction between BMMCs and the mesentery was examined by using mast cell deficient WBB6F1(F1)-W/Wv [c-kit receptor tyrosine kinase (KIT) mutant], F1-Sl/Sld [KIT ligand stem cell factor mutant], and F1-tg/tg [a practically microphthalmia transcription factor (MITF)-null mutant] mice. Three parameters were measured: the number of BMMCs: (1) developed in the mesentery 5 weeks after intraperitoneal injection into mast cell deficient mice, (2) adhered to mesenteric mesothelial cells, and (3) transmigrated across the mesenteric mesothelial cell monolayer when coculturing both cells for 3 and 18 h, respectively. After intraperitoneal injection, F1-wild type (+/+) BMMCs developed in the mesentery of F1-W/Wv mice but not in that of F1-Sl/Sld mice, while F1-tg/tg BMMCs did not develop, even in the mesentery of WBB6F1-W/Wv mice. In the coculture, WB-W/W BMMCs normally adhered to but poorly transmigrated across F1-+/+ mesothelial cells, and in accordance, F1-+/+ BMMCs normally adhered to but poorly transmigrated across F1-Sl/Sld mesothelial cells. F1-tg/tg BMMCs showed poor adhesion and transmigration, but both parameters were partially but significantly improved by ectopic expression of spermatogenic immunoglobulin superfamily (SgIGSF), a mast-cell adhesion molecule critically regulated by MITF. Since F1-tg/tg BMMCs expressed reduced levels of KIT, these results suggested that SgIGSF and KIT independently played a significant role in the transmigration. Among three parameters, development of mast cells in the mesentery well correlated with the transmigration. This process seemed important for mast cells to settle down from the peritoneal cavity to the mesentery.
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PMID:Distinct roles for the SgIGSF adhesion molecule and c-kit receptor tyrosine kinase in the interaction between mast cells and the mesentery. 1547 95