Báo cáo y học: "Neutrophil ‘connectivity’: key to neutrophil-mediated tissue injury"

Tuyển tập các báo cáo nghiên cứu về y học được đăng trên tạp chí y học Critical Care giúp cho các bạn có thêm kiến thức về y học đề tài: Neutrophil ‘connectivity’: key to neutrophil-mediated tissue injury? | Available online http content 7 4 285 Commentary Neutrophil connectivity key to neutrophil-mediated tissue injury Salahaddin Mahmudi-Azer1 and Stephan F van Eeden2 Senior Post-Doctoral fellow Department of Medicine University of British Columbia . McDonald Research Laboratory iCAPTURE Centre St Paul s Hospital Vancouver BC Canada 2Associate Professor Department of Medicine University of British Columbia . McDonald Research Laboratory CAPTURE Centre St Paul s Hospital Vancouver BC Canada Correspondence Stephan F van Eeden svaneeden@ Published online 24 February 2003 Critical Care 2003 7 285-287 DOI cc1884 This article is online at http content 7 4 285 2003 BioMed Central Ltd Print ISSN 1364-8535 Online ISSN 1466-609X Abstract Neutrophils use cell surface molecules to communicate with their external environment. These molecules are markers reflecting neutrophil development activation status and cell function. They are also critically important in controlling neutrophil behavior. Targeting these cell surface molecules is an attractive approach in the treatment of neutrophil-mediated conditions. Keywords connectivity inflammation neutrophils surface molecules tissue injury Neutrophils are professional phagocytic cells that provide the host with a first line of defense against acute bacterial and fungal diseases. They sense the focus of infection they adhere to the endothelium of capillaries and venules adjacent to the inflammatory locus they migrate through the vessel wall and the interstitial tissues to the infectious site and they phagocytose kill and digest the invading microorganisms using a large number of proinflammatory mediators and proteolytic enzymes. During the inflammatory process neutrophils produce factors to ensure their survival in the hostile inflammatory milieu they recruit additional phagocytes they inactivate their own toxic products and they induce their own death pathway to prevent damage to .

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