Molecular and cellular basis of Bartonella pathogenesis

被引:144
作者
Dehio, C [1 ]
机构
[1] Univ Basel, Biozentrum, Dept Mol Microbiol, CH-4056 Basel, Switzerland
关键词
cell proliferation; antiapoptosis; invasion; endothelial cell; erythrocyte; type IV secretion system;
D O I
10.1146/annurev.micro.58.030603.123700
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
The genus Bartonella comprises several important human pathogens that cause a wide range of clinical manifestations: cat-scratch disease, trench fever, Carrion's disease, bacteremia with fever, bacillary angiomatosis and peliosis, endocarditis, and neuroretinitis. Common features of bartonellae include transmission by blood-sucking arthropods and the specific interaction with endothelial cells and erythrocytes of their mammalian hosts. For each Bartonella species, the invasion and persistent intracellular colonization of erythrocytes are limited to a specific human or animal reservoir host. In contrast, endothelial cells are target host cells in probably all mammals, including humans. Bartonellae subvert multiple cellular functions of human endothelial cells, resulting in cell invasion, proinflammatory activation, suppression of apoptosis, and stimulation of proliferation, which may cumulate in vasoproliferative tumor growth. This review summarizes our understanding of Bartonella-host cell interactions and the molecular mechanisms of bacterial virulence and persistence. In addition, current controversies and unanswered questions in this area are highlighted.
引用
收藏
页码:365 / 390
页数:26
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