Abstract
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 HCO3- 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 HCO3- 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 HCO3- production/secretion, which requires CFTR expression in lymphocytes.
Original language | English |
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Pages (from-to) | 3887-3894 |
Number of pages | 8 |
Journal | Journal of Cellular Physiology |
Volume | 227 |
Issue number | 12 |
DOIs | |
Publication status | Published - 1 Dec 2012 |
Externally published | Yes |
ASJC Scopus subject areas
- Physiology
- Clinical Biochemistry
- Cell Biology