期刊
RESPIRATORY RESEARCH
卷 9, 期 -, 页码 -出版社
BMC
DOI: 10.1186/1465-9921-9-82
关键词
-
资金
- Natural Sciences Foundation of China
- Beijing Natural Sciences Foundation
- Education Ministry of China New Century Excellent Talent
- Key Laboratory of Comparative Medicine of Healthy Ministry [30470767, 7072063, NCET 06-0156, ZDS 200805]
Background: CD8+ T cells may participate in cigarette smoke (CS) induced-lung inflammation in mice. CXCL10/IP-10 (IFN gamma-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 IFN gamma and CXCR3 ligands (particularly CXCL10). Conclusion: Our findings show that CXCR3 is important in promoting CD8+ T cell recruitment and in initiating IFN gamma and CXCL10 release following CS exposure. CXCR3 may represent a promising therapeutic target for acute lung inflammation induced by CS.
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