Intracellular survival of Burkholderia cepacia complex isolates in the presence of macrophage cell activation

被引:97
作者
Saini, LS
Galsworthy, SB
John, MA
Valvano, MA [1 ]
机构
[1] Univ Western Ontario, Dept Microbiol & Immunol, London, ON N6A 5C1, Canada
[2] Univ Western Ontario, Dept Med, London, ON N6A 5C1, Canada
[3] London Hlth Sci Ctr, Dept Microbiol & Infect Control, London, ON N6A 4G5, Canada
来源
MICROBIOLOGY-UK | 1999年 / 145卷
关键词
Burkholderia cepacia; macrophage activation; intracellular survival; cystic fibrosis;
D O I
10.1099/00221287-145-12-3465
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
Strains of the Burkholderia cepacia complex have emerged as a serious threat to patients with cystic fibrosis due to their ability to infect the lung and cause, in some patients, a necrotizing pneumonia that is often lethal. It has recently been shown that several strains of the B. cepacia complex can escape intracellular killing by free-living amoebae following phagocytosis. In this work, the ability of two B, cepacia complex strains to resist killing by macrophages was explored, Using fluorescence microscopy, electron microscopy and a modified version of the gentamicin-protection assay, we demonstrate that B, cepacia CEP021 (genomovar VI), and Burkholderia vietnamiensis (previously B. cepacia genomovar V) CEP040 can survive in PU5-1.8 murine macrophages for a period of at least Sd without significant bacterial replication. Furthermore, bacterial entry into macrophages stimulated production of tumour necrosis factor and primed them to release toxic oxygen radicals following treatment with phorbol myristoyl acetate. These effects were probably caused by bacterial LPS, as they were blocked by polymyxin B, Infected macrophages primed with interferon gamma produced less nitric oxide than interferon-gamma-primed uninfected cells. We propose that the ability of B. cepacia to resist intracellular killing by phagocytic cells may play a role in the pathogenesis of cystic fibrosis lung infection. Our data are consistent with a model where repeated cycles of phagocytosis and cellular activation without bacterial killing may promote a deleterious inflammatory response causing tissue destruction and decay of lung function.
引用
收藏
页码:3465 / 3475
页数:11
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