Attenuation of Acute Lung Inflammation Induced by Cigarette Smoke in CXCR3 Knockout Mice

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Attenuation of Acute Lung Inflammation Induced by Cigarette Smoke in CXCR3 Knockout Mice

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Title: Attenuation of Acute Lung Inflammation Induced by Cigarette Smoke in CXCR3 Knockout Mice
Author: Nie, Li; Xiang, Ruolan; Zhou, Weixun; Cheng, Deyun; Gao, Jinming; Lu, Bao

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Citation: Nie, Li, Ruolan Xiang, Weixun Zhou, Bao Lu, Deyun Cheng, and Jinming Gao. 2008. Attenuation of acute lung inflammation induced by cigarette smoke in CXCR3 knockout mice. Respiratory Research 9:82.
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Abstract: Background: CD8+ T cells may participate in cigarette smoke (CS) induced-lung inflammation in mice. CXCL10/IP-10 (IFNγ-inducible protein 10) and CXCL9/Mig (monokine induced by IFN-\(\gamma\)) are up-regulated in CS-induced lung injury and may attract T-cell recruitment to the lung. These chemokines together with CXCL11/ITAC (IFN-inducible T-cell alpha chemoattractant) are ligands for the chemokine receptor CXCR3 which is preferentially expressed chiefly in activated CD8+ T cells. The purpose of this investigation was to study the contribution of CXCR3 to acute lung inflammation induced by CS using CXCR3 knockout (KO) mice. Methods: Mice (n = 8 per group) were placed in a closed plastic box connected to a smoke generator and were exposed whole body to the tobacco smoke of five cigarettes four times a day for three days. Lung pathological changes, expression of inflammatory mediators in bronchoalveolar lavage (BAL) fluid and lungs at mRNA and protein levels, and lung infiltration of CD8+ T cells were compared between CXCR3-/- mice and wild type (WT) mice. Results: Compared with the WT littermates, CXCR3 KO mice showed less CS-induced lung inflammation as evidenced by less infiltration of inflammatory cells in airways and lung tissue, particularly fewer CD8+ T cells, lower levels of IFNγ and CXCR3 ligands (particularly CXCL10). Conclusion: Our findings show that CXCR3 is important in promoting CD8+ T cell recruitment and in initiating IFNγ and CXCL10 release following CS exposure. CXCR3 may represent a promising therapeutic target for acute lung inflammation induced by CS.
Published Version: doi:10.1186/1465-9921-9-82
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2654035/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:10202478
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