PT  - JOURNAL ARTICLE
AU  - Bo Li
AU  - Chunling Dong
AU  - Guifang Wang
AU  - Huiru Zheng
AU  - Xiangdong Wang
AU  - Chunxue Bai
TI  - Pulmonary epithelial CCR3 promotes LPS-induced lung inflammation by mediating release of IL-8
DP  - 2011 Sep 01
TA  - European Respiratory Journal
PG  - 2939
VI  - 38
IP  - Suppl 55
4099  - http://erj.ersjournals.com/content/38/Suppl_55/2939.short
4100  - http://erj.ersjournals.com/content/38/Suppl_55/2939.full
SO  - Eur Respir J2011 Sep 01; 38
AB  - Objectives: Interleukin (IL)-8 from pulmonary epithelial cells has been suggested to play an important role in the airway inflammation, although the mechanism remains unclear. We envisioned a possibility that pulmonary epithelial CCR3 could be involved in secretion and regulation of IL-8 and promote Lipopolysaccharide (LPS)-induced lung inflammation.Methods: Human bronchial epithelial cell line NCI-H292 and alveolar type II epithelial cell line A549 were used to test role of CCR3 in production of IL-8 at cellular level. In vivo studies were performed on C57/BL6 mice instilled intratracheally with LPS in a model of acute lung injury (ALI). The activity of a CCR3-specific inhibitor (SB-328437) was measured in both in vitro and in vivo systems.Results: We found that expressions of CCR3 on NCI-H292 and A549 cells were increased by 23% and 16%, respectively, 24 h after the challenge with LPS. LPS increased IL-8 productions in NCI-H292 and A549 cells, which were inhibited significantly by SB-328437. SB-328437 also diminished neutrophil recruitment in alveolar airspaces and improved LPS-induced ALI accompanied with reduction of IL-8 secretion in bronchoalveolar lavage fluid.Conclusions: These results suggest that pulmonary epithelial CCR3 be involved in progression of LPS-induced lung inflammation by mediating release of IL-8. CCR3 in pulmonary epithelia may be an attractive target for development of therapies for ALI.