Lymphocyte CFTR promotes epithelial bicarbonate secretion for bacterial killing

Xiao Xiao Tang, Kin Lam Fok, Hao Chen, Kay Sheung Chan, Lai Ling Tsang, Dewi Kenneth Rowlands, Xiao Hu Zhang, Jian Da Dong, Yechun Ruan, Xiaohua Jiang, Sidney Siu Bun Yu, Yiu Wa Chung, Hsiao Chang Chan

Research output: Journal article publicationJournal articleAcademic researchpeer-review

18 Citations (Scopus)


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 languageEnglish
Pages (from-to)3887-3894
Number of pages8
JournalJournal of Cellular Physiology
Issue number12
Publication statusPublished - 1 Dec 2012
Externally publishedYes

ASJC Scopus subject areas

  • Physiology
  • Clinical Biochemistry
  • Cell Biology


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