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- Title
Bartonella henselae trimeric autotransporter adhesin BadA expression interferes with effector translocation by the VirB/ D4 type IV secretion system.
- Authors
Lu, Yun‐Yueh; Franz, Bettina; Truttmann, Matthias C.; Riess, Tanja; Gay‐Fraret, Jérémie; Faustmann, Marco; Kempf, Volkhard A. J.; Dehio, Christoph
- Abstract
The Gram-negative, zoonotic pathogen Bartonella henselae is the aetiological agent of cat scratch disease, bacillary angiomatosis and peliosis hepatis in humans. Two pathogenicity factors of B. henselae - each displaying multiple functions in host cell interaction - have been characterized in greater detail: the trimeric autotransporter Bartonella adhesin A ( BadA) and the type IV secretion system VirB/ D4 ( VirB/ D4 T4 SS). BadA mediates, e.g. binding to fibronectin ( Fn), adherence to endothelial cells ( ECs) and secretion of vascular endothelial growth factor ( VEGF). VirB/ D4 translocates several Bartonella effector proteins ( Beps) into the cytoplasm of infected ECs, resulting, e.g. in uptake of bacterial aggregates via the invasome structure, inhibition of apoptosis and activation of a proangiogenic phenotype. Despite this knowledge of the individual activities of BadA or VirB/ D4 it is unknown whether these major virulence factors affect each other in their specific activities. In this study, expression and function of BadA and VirB/D4 were analysed in a variety of clinical B. henselae isolates. Data revealed that mostisolates have lost expression of either BadA or VirB/ D4 during in vitro passages. However, the phenotypic effects of coexpression of both virulence factors was studied in one clinical isolate that was found to stably coexpress BadA and VirB/ D4, as well as by ectopic expression of BadA in a strain expressing VirB/ D4 but not BadA. BadA, which forms a dense layer on the bacterial surface, negatively affected VirB/ D4-dependent Bep translocation and invasome formation by likely preventing close contact between the bacterial cell envelope and the host cell membrane. In contrast, BadA-dependent Fn binding, adhesion to ECs and VEGF secretion were not affected by a functional VirB/ D4 T4 SS. The obtained data imply that the essential virulence factors BadA and VirB/ D4 are likely differentially expressed during different stages of the infection cycle of Bartonella.
- Subjects
BARTONELLA henselae; GENE expression; CHROMOSOMAL translocation; ETIOLOGY of diseases; ENDOTHELIAL cells; FIBRONECTINS; APOPTOSIS; SECRETION
- Publication
Cellular Microbiology, 2013, Vol 15, Issue 5, p759
- ISSN
1462-5814
- Publication type
Article
- DOI
10.1111/cmi.12070