TAILIEUCHUNG - Báo cáo khoa học: Bacterial-induced hepoxilin A3 secretion as a pro-inflammatory mediator

Bacterial infections at epithelial surfaces, such as those that line the gut and the lung, stimulate the migration of neutrophils through the co-ordi-nated actions of chemoattractants secreted from pathogen-stimulated epi-thelial cells. One such factor involved in attracting polymorphonuclear leukocytes across the epithelium and into the lumen has until recently remained elusive. | ỊFEBS Journal MINIREVIEW Bacterial-induced hepoxilin A3 secretion as a pro-inflammatory mediator Beth A. McCormick Department of Pediatric Gastroenterology Massachusetts General Hospital and Department of Microbiology and Molecular Genetics Harvard Medical School Charlestown MA USA Keywords arachidonic acid chemotaxis eicosanoid hepoxolin A3 inflammation intestine lung neutrophils Pseudomonas aeruginosa Salmonella typhimurium Correspondence B. A. McCormick Department of Pediatric Gastroenterology Massachusetts General Hospital Harvard Medical School CNY 114 16th Street 114-3503 Charlestown MA 02129 USA Fax 1 617 7264172 Tel 1 617 7264168 E-mail mccormic@ Received 13 Oct 2006 accepted 23 May 2007 doi Bacterial infections at epithelial surfaces such as those that line the gut and the lung stimulate the migration of neutrophils through the co-ordinated actions of chemoattractants secreted from pathogen-stimulated epithelial cells. One such factor involved in attracting polymorphonuclear leukocytes across the epithelium and into the lumen has until recently remained elusive. In 2004 we identified the eicosanoid hepoxilin A3 to be selectively secreted from the apical surface of human intestinal or lung epithelial cells stimulated with Salmonella enterica serotype Typhimurium or Pseudomonas aeruginosa respectively. In this role the function of hepoxilin A3 is to guide neutrophils via the establishment of a gradient across the epithelial tight junction complex. Interestingly interruption of the synthetic pathway of hepoxilin A3 blocks the apical release of hepoxilin A3 in vitro and the transmigration of neutrophils induced by S. typhimurium both in in vitro and in vivo models of inflammation. Such results have led to the discovery of a completely novel pathway that is not only critical for responses to bacterial pathogens but also has broad implications for inflammatory responses affecting mucosal surfaces in general.

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