Open AccessPro‐inflammatory effects of Burkholderia cepacia on cystic fibrosis respiratory epithelium
Author(s) -
Fink Joshua,
Steer James H,
Joyce David A,
McWilliam Andrew S,
Stewart Geoffrey A
Publication year - 2003
Publication title -
fems immunology & medical microbiology
Language(s) - English
Resource type - Journals
eISSN - 1574-695X
pISSN - 0928-8244
DOI - 10.1016/s0928-8244(03)00169-x
Subject(s) - biology , cystic fibrosis transmembrane conductance regulator , burkholderia , cytokine , cystic fibrosis , respiratory epithelium , epithelium , cell culture , immunology , microbiology and biotechnology , interleukin 8 , genetics , bacteria
Burkholderia cepacia causes pulmonary infection with high mortality in cystic fibrosis (CF) patients which is likely to involve interaction with respiratory epithelium. In this study the pro‐inflammatory properties of B. cepacia were examined using a range of respiratory epithelial cell lines. B. cepacia and cell‐free culture supernatants were used to stimulate cell lines with (ΣCFTE29o‐ and IB3) and without (A549) the CF transmembrane conductance regulator mutation (CFTR), together with corrected cell lines (C38 and S9). Interleukin (IL)‐6 and IL‐8, but not GM‐CSF or IL‐1β, were released from all the cell lines whereas PGE 2 (prostaglandin E 2 ) was released from the A549, IB3 and S9 cell lines only. Nuclear factor (NF)‐κB activation preceded cytokine release and suppression of NF‐κB activity diminished cytokine release. These studies indicated that B. cepacia secretory products are potent pro‐inflammatory agents for respiratory epithelium and suggest functional CFTR is not required for cytokine or prostanoid responses.