Lymphocyte CFTR promotes epithelial bicarbonate secretion for bacterial killing.
J Cell Physiol
; 227(12): 3887-94, 2012 Dec.
Article
em En
| MEDLINE
| ID: mdl-22552906
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 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.
Texto completo:
1
Coleções:
01-internacional
Base de dados:
MEDLINE
Assunto principal:
Bicarbonatos
/
Linfócitos
/
Regulador de Condutância Transmembrana em Fibrose Cística
Limite:
Animals
/
Humans
Idioma:
En
Revista:
J Cell Physiol
Ano de publicação:
2012
Tipo de documento:
Article
País de afiliação:
China