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

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Cellular & Molecular Immunology 2011年第4期8卷 305-314页

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 Department of Regional Cooperation for Infectious Diseases Tohoku University Graduate School of MedicineSendaiMiyagiJapan Department of Advanced Preventive Medicine for Infectious Disease Tohoku University Graduate School of MedicineSendaiMiyagiJapan Department of Respiratory Medicine Japanese Red-Cross Ishinomaki HospitalIshinomakiMiyagiJapan Department of Infection Control and Laboratory Diagnostics Tohoku University Graduate School of MedicineSendaiMiyagiJapan Department of Clinical Microbiology with Epidemiological Research&Management and Analysis of Infectious Diseases Tohoku University Graduate School of MedicineSendaiMiyagiJapan Institute of Biomaterials and Bioengineering Tokyo Medical and Dental UniversityChiyoda-kuTokyoJapan Graduate School of Pharmaceutical Sciences Kyoto UniversityKyotoJapan

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.

关键词： CXCL12 CXCR4 lipopolysaccharides lung injury neutrophils

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