Influences of influenza virus on cystic fibrosis transmembrane conductance regulator ( CFTR)
10.3760/cma.j.issn.0254-5101.2017.11.001
- VernacularTitle:流感病毒对囊性纤维化跨膜转导调节因子影响的研究
- Author:
Yapeng HOU
1
;
Zhiyu ZHOU
;
Jianjun CHANG
;
Yan DING
;
Hongguang NIE
Author Information
1. 中国医科大学代谢病分子机制与药物研究所
- Keywords:
Influenza virus;
Mouse tracheal epithelial cell;
Cystic fibrosis transmembrane con-ductance regulator;
Short-circuit current
- From:
Chinese Journal of Microbiology and Immunology
2017;37(11):805-809
- CountryChina
- Language:Chinese
-
Abstract:
Objective To evaluate the differentiation of mouse tracheal epithelial cells ( MTEC) at an air-liquid interface and to investigate the influences of influenza virus on the cystic fibrosis transmem-brane conductance regulator ( CFTR) in primary cultured MTEC for further elucidating the possible mecha-nism of imbalanced fluid and salt transportation in respiratory system caused by influenza virus infection . Methods The morphology of primarily cultured MTEC was observed under inverted microscope .Trans epi-thelial electrical resistance ( TEER) was measured by a resistance meter to evaluate the integrity of cultured MTEC.An Ussing chamber apparatus was used to record the short-circuit current of primary cultured MTEC . Results The primarily cultured MTEC clustered together and had a tight pavement-like appearance under light microscope .The TEER was greater than 1000 Ωafter 6 days of culture .Influenza virus could reduce the short-circuit current of CFTR to (52.77±10.30)％in intact cell membrane and to (41.50±1.09)％in monolayer MTEC after increasing the permeability of basement membrane .It had been proved that CFTR was essential to maintaining the balance of fluid and salt transportation in respiratory system.Conclusion Mouse MTEC are efficiently cultured at a air-liquid interface and the primarily cultured cells are highly simi-lar to those in a normal physiologic state .Influenza virus may block the secretion of anions through inhibiting the function of CFTR , which may induce the development of chronic obstructive pulmonary disease and the incidence of asthma .
