期刊
JOURNAL OF CELLULAR PHYSIOLOGY
卷 227, 期 12, 页码 3887-3894出版社
WILEY-BLACKWELL
DOI: 10.1002/jcp.24101
关键词
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资金
- National Natural Science Foundation
- National 973 project [2009CB522102]
- Focused Investment Scheme
- Li Ka Shing Institute of Health Sciences of The Chinese University of Hong Kong
The expression of cystic fibrosis transmembrane conductance regulator (CFTR) in lymphocytes has been reported for nearly two decades; however, its physiological role remains elusive. Here, we report that co-culture of lymphocytes with lung epithelial cell line, Calu-3, promotes epithelial HCO?3- production/secretion with up-regulated expression of carbonic anhydrase 2 and 4 (CA-2, CA-4) and enhanced bacterial killing capability. The lymphocyte-enhanced epithelial HCO?3- secretion and bacterial killing activity was abolished when Calu3 cells were co-cultured with lymphocytes from CFTR knockout mice, or significantly reduced by interfering with E-cadherin, a putative binding partner of CFTR. Bacterial lipopolysaccharide (LPS)-induced E-cadherin and CA-4 expression in the challenged lung was also found to be impaired in CFTR knockout mice compared to that of the wild-type. These results suggest that the interaction between lymphocytes and epithelial cells may induce a previously unsuspected innate host defense mechanism against bacterial infection by stimulating epithelial HCO?3- production/secretion, which requires CFTR expression in lymphocytes. J. Cell. Physiol. 227: 38873894, 2012. (c) 2012 Wiley Periodicals, Inc.
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