The increase in surface CXCR4 expression on lung extravascular neutrophils and its effects on neutrophils during endotoxin-induced lung injury

作     者：Mitsuhiro Yamada Hiroshi Kubo Seiichi Kobayashi Kota Ishizawa Mei He Takaya Suzuki Naoya Fujino Hiroyuki Kunishima Masamitsu Hatta Katsushi Nishimaki Tetsuji Aoyagi Kouichi Tokuda Miho Kitagawa Hisakazu Yano Hirokazu Tamamura Nobutaka Fujii Mitsuo Kaku 

作者机构：Department of Regional Cooperation for Infectious DiseasesTohoku University Graduate School of MedicineSendaiMiyagiJapan Department of Advanced Preventive Medicine for Infectious DiseaseTohoku University Graduate School of MedicineSendaiMiyagiJapan Department of Respiratory MedicineJapanese Red-Cross Ishinomaki HospitalIshinomakiMiyagiJapan Department of Infection Control and Laboratory DiagnosticsTohoku University Graduate School of MedicineSendaiMiyagiJapan Department of Clinical Microbiology with Epidemiological Research&Management and Analysis of Infectious DiseasesTohoku University Graduate School of MedicineSendaiMiyagiJapan Institute of Biomaterials and BioengineeringTokyo Medical and Dental UniversityChiyoda-kuTokyoJapan Graduate School of Pharmaceutical SciencesKyoto UniversityKyotoJapan 

出 版 物：《Cellular & Molecular Immunology》 (中国免疫学杂志（英文版）)

年 卷 期：2011年第8卷第4期

页      面：305-314页

核心收录：

学科分类：1002[医学-临床医学] 100214[医学-肿瘤学] 10[医学] 

基　　金：grants from the Japanese Society for the Promotion of Science(no.17590776 to HK and no.17790524 to MY) 

主　　题：CXCL12 CXCR4 lipopolysaccharides lung injury neutrophils 

摘      要：Inflammatory stimuli,such as a microbes or lipopolysaccharides,induce a rapid release of neutrophils from the bone marrow and promote neutrophil migration into inflamed sites to promote host ***,an excess accumulation and retention of neutrophils in inflamed tissue can cause severe tissue injuries in the later stages of *** studies have reported that both CXCL12 levels in injured lungs and its receptor,CXCR4,on accumulated neutrophils in injured lungs,increased;furthermore,these studies showed that the CXCL12/CXCR4 signaling pathway participated in neutrophil accumulation in the later stages of lipopolysaccharide(LPS)-induced lung ***,the mechanisms underlying this increase in surface CXCR4 expression in neutrophils remain *** this study,we found that surface CXCR4 expression increased in extravascular,but not intravascular,neutrophils in the lungs of LPS-induced lung injury model ***,ex vivo studies revealed that CXCL12 acted not only as a chemoattractant,but also as a suppressor of cell death for the lung neutrophils expressing ***,one of the native ligands for L-selectin,induced the increase of surface CXCR4 expression on isolated circulating neutrophils,suggesting that the activation of L-selectin may be involved in the increase in surface *** findings show that surface CXCR4 levels on neutrophils increase after extravasation into injured lungs,possibly through the activation of *** CXCL12/CXCR4 signaling pathway plays an important role in the modulation of neutrophil activity during acute lung injury,not only by promoting chemotaxis but also by suppressing cell death.