Bo Li and Chunling Dong contributed equally to this work.
Original Research Article
Pulmonary epithelial CCR3 promotes LPS-induced lung inflammation by mediating release of IL-8
Article first published online: 9 JUN 2011
Copyright © 2011 Wiley-Liss, Inc.
Journal of Cellular Physiology
Volume 226, Issue 9, pages 2398–2405, September 2011
How to Cite
Li, B., Dong, C., Wang, G., Zheng, H., Wang, X. and Bai, C. (2011), Pulmonary epithelial CCR3 promotes LPS-induced lung inflammation by mediating release of IL-8. J. Cell. Physiol., 226: 2398–2405. doi: 10.1002/jcp.22577
- Issue published online: 9 JUN 2011
- Article first published online: 9 JUN 2011
- Accepted manuscript online: 9 DEC 2010 12:00AM EST
- Manuscript Accepted: 24 NOV 2010
- Manuscript Received: 21 APR 2010
- Shanghai Leading Academic Discipline Project. Grant Number: B115
- Fudan University
- Shanghai Science and Technology Committee. Grant Number: 08PJ1402900, 08DZ2293104, 9540702600
- National Natural Science Foundation of China. Grant Number: 30370611
- Program for Outstanding Medical Academic Leader of Shanghai. Grant Number: LJ06022
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. 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. We found that expression of CCR3 in NCI-H292 and A549 cells were increased by 23% and 16%, respectively, 24 h after the challenge with LPS. LPS increased the expression of CCR3 in NCI-H292 and A549 cells in a time-dependent manner, which was inhibited significantly by SB-328437. SB-328437 also diminished neutrophil recruitment in alveolar airspaces and improved LPS-induced ALI and production of IL-8 in bronchoalveolar lavage fluid. 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. J. Cell. Physiol. 226: 2398–2405, 2011. © 2010 Wiley-Liss, Inc.