| Title | Acute pulmonary inflammation is inhibited in CXCR3 knockout mice after short-term cigarette smoke exposure |
| Authors | Nie, Li Xiang, Ruo-lan Liu, Yong Zhou, Wei-xun Jiang, Lei Lu, Bao Pang, Bao-sen Cheng, De-yun Gao, Jin-ming |
| Affiliation | Chinese Acad Med Sci, Dept Resp Dis, Peking Union Med Coll Hosp, Beijing 100730, Peoples R China. Chinese Acad Med Sci, Dept Pathol, Peking Union Med Coll Hosp, Beijing 100730, Peoples R China. Peking Union Med Coll, Beijing 100730, Peoples R China. Sichuan Univ, Dept Resp Dis, W China Hosp, Chengdu 610041, Peoples R China. Peking Univ, Hlth Sci Ctr, Dept Pathophysiol, Beijing 100088, Peoples R China. Harvard Univ, Sch Med, Ina Sue Perlmutter Lab, Boston, MA 02115 USA. Capital Med Univ, Resp Inst, Beijing 100020, Peoples R China. |
| Keywords | CXCR3 CD8 CXCL10 cigarette smoke CHEMOKINE RECEPTOR CXCR3 PERIPHERAL AIRWAYS LUNG INFLAMMATION INDUCED EMPHYSEMA T-LYMPHOCYTES DISEASE EXPRESSION INDUCTION CYTOKINE SPUTUM |
| Issue Date | 2008 |
| Publisher | 中国药理学报 |
| Citation | ACTA PHARMACOLOGICA SINICA.2008,29,(12),1432-1439. |
| Abstract | Aim: CXCR3, via binding its specific ligand CXCL10, plays an important role in cigarette smoke (CS)-induced pulmonary inflammation. CXCR3 is preferentially expressed in activated T cells (chiefly CD8(+) T cells). The purpose of this study was to investigate the role of CXCR3 in CS-induced pulmonary injury using CXCR3 gene-deficient (CXCR3-/-) mice. Methods: Differences in the infiltration of inflammator cells and CD8(+) T cells and the expression of inflammatory mediators and chemokines in the bronchoalveolar lavage fluid and lungs at the mRNA and protein levels were compared between CXCR3-/- mice and wild-type (WT) mice at 2 h after 3 d of CS exposure. Results: Compared with their WT counterparts, the CXCR3-/- mice showed alleviated inflammation, as evidenced by fewer inflammatory cells, particularly cytotoxic CD8(+) T cells, in bronchoalveolar lavage fluid and lung tissues. At both the mRNA and protein levels, there were significantly lower levels of inflammatory and chemotactic cytokines, including TNF-alpha, interleukin-8, interferon-gamma, transforming growth factor-beta 1, and CXCL10 in the CXCR3-/- mice. Conclusion: Our data show that CXCR3 is important in recruiting inflammatory cells (particularly CD8(+) T cells) into the airways and lungs, as well as initiating inflammatory and fibrotic cytokines release at 2 h following a short-term CS insult. CXCR3 could be a novel target for the treatment of pulmonary inflammation induced by CS. |
| URI | http://hdl.handle.net/20.500.11897/397068 |
| ISSN | 1671-4083 |
| DOI | 10.1111/j.1745-7254.2008.00899.x |
| Indexed | SCI(E) 中国科技核心期刊(ISTIC) 中国科学引文数据库(CSCD) |
| Appears in Collections: | 医学部待认领 |
