Differences in invasion and translocation of Burkholderia cepacia complex species in polarised lung epithelial cells in vitro

被引:43
作者
Duff, Caroline
Murphy, Philip G.
Callaghan, Maire
McClean, Siobhan
机构
[1] Inst Technol Tallaght, Dept Appl Sci, Dublin 24, Ireland
[2] Inst Technol Tallaght, Natl Inst Cellular Biotechnol, Dublin 24, Ireland
[3] Adelaide Meath & Natl Childrens Hosp, Dublin 24, Ireland
关键词
Burkholderia cepacia complex; lung epithelial cells; tight junctions; bacterial invasion; translocation;
D O I
10.1016/j.micpath.2006.07.005
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
In order to investigate the mechanisms by which Burkholderia cepacia complex (Bee) strains cross the epithelial barrier of the lung and cause septicaemia in a subgroup of Cystic Fibrosis (CF) patients, the invasiveness of four Bee species have been examined in three lung epithelial cells: A549, 16HBE14o- and Calu-3. The latter two cell lines form polarised monolayers when grown on filters. Invasion of both cell lines by B. multivorans strains was reduced when the cells were grown as tight monolayers compared unpolarised cells, suggesting basolateral receptors are required for the process. In contrast, four B. cenocepacia strains showed comparable invasion of both cell lines irrespective of culture model. All four species of Bee reduced the TER of Calu-3 monotayers. However, while B. cepacia, B. multivorans and B. stabilis strains readily translocated across the epithelial monolayer, B. cenocepacia translocation was slower. Both B. multivorans and B. cenocepacia altered expression of ZO-1 in Calu-3 cells, but not E-cadherin. Overall, the findings that Bee strains from four species, which differ greatly in their virulence, have the potential to disrupt tight junctions and to translocate across the epithelium, demonstrates this effect is not exclusive to the most virulent species. (c) 2006 Elsevier Ltd. All rights reserved.
引用
收藏
页码:183 / 192
页数:10
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