P. aeruginosa LPS stimulates calcium signaling and chloride secretion via CFTR in human bronchial epithelial cells.
BACKGROUND
Pseudomonas aeruginosa airway infection is associated with a high mortality rate in cystic fibrosis. Lipopolysaccharide (LPS), a main constituent of the outer membrane of P. aeruginosa, is responsible for activation of innate immune response but its role on airway epithelium ion transport, is not well known. The aim of this study was to determine the role for P. aeruginosa LPS in modulating chloride secretion and intracellular calcium in the human bronchial epithelial cell line, 16HBE14o-.


METHODS
We used intracellular calcium imaging and short-circuit current measurement upon exposure of cells to P. aeruginosa LPS.


RESULTS
Apical LPS stimulated intracellular calcium release and calcium entry and enhanced chloride secretion. This latter effect was significantly inhibited by CFTR(inh)-172 and BAPTA-AM (intracellular Ca(2+) chelator).


CONCLUSIONS
Our data provides evidence for a new role of P. aeruginosa LPS in stimulating calcium entry and release and a subsequent chloride secretion via CFTR in human bronchial epithelium.
Laboratoire de Physiologie, EA2689, IMPRT IFR 114, Université de Lille, Lille cedex, France. julien.buyck@uclouvain.be
J M
JM
Buyck
V
V
Verriere
R
R
Benmahdi
G
G
Higgins
B
B
Guery
R
R
Matran
B J
BJ
Harvey
K
K
Faure
V
V
Urbach
D001693:Biological Transport, Active / Q000187:drug effects; D001980:Bronchi / Q000166:cytology*; D002118:Calcium / Q000378:metabolism*; D002712:Chlorides / Q000378:metabolism*; D019005:Cystic Fibrosis Transmembrane Conductance Regulator / Q000502:physiology*; D004847:Epithelial Cells / Q000502:physiology*; D006801:Humans; D008070:Lipopolysaccharides / Q000502:physiology*; D011550:Pseudomonas aeruginosa
C505032:CFTR protein, human; D002712:Chlorides; D008070:Lipopolysaccharides; D019005:Cystic Fibrosis Transmembrane Conductance Regulator; D002118:Calcium