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          Institute: MPI für Entwicklungsbiologie     Collection: Abteilung 1 - Protein Evolution (A. Lupas)     Display Documents

ID: 305920.0, MPI für Entwicklungsbiologie / Abteilung 1 - Protein Evolution (A. Lupas)
Bartonella quintana variably expressed outer membrane proteins mediate vascular endothelial growth factor secretion but not host cell adherence.
Authors:Schulte, B.; Linke, Dirk; Klumpp, S.; Schaller, M.; Riess, T.; Autenriedth, Ingo; Kempf, V. A. J.
Date of Publication (YYYY-MM-DD):2006-09
Title of Journal:Infect Immun. 2006 Sep;74(9):5003-13.
Issue / Number:(9)
Start Page:5003
End Page:5013
Sequence Number of Article:16926391
Review Status:not specified
Audience:Not Specified
Abstract / Description:Bartonella quintana causes trench fever, endocarditis, and the vasculoproliferative disorders bacillary angiomatosis and peliosis hepatis in humans. Little is known about the interaction of this pathogen with host cells. We attempted to elucidate the interaction of B. quintana with human macrophages (THP-1) and epithelial cells (HeLa 229). Remarkably, only B. quintana strain JK-31 induced secretion of vascular endothelial growth factor (VEGF) from THP-1 and HeLa 229 cells upon infection similar to the secretion induced by B. henselae Marseille, whereas other strains (B. quintana 2-D70, B. quintana Toulouse, and B. quintana Munich) did not induce such secretion. Immunofluorescence testing and electron microscopy revealed that the B. quintana strains unable to induce VEGF secretion did not express the variable outer membrane proteins (Vomps) on their surfaces. Surprisingly, the increase in VEGF secretion mediated by B. quintana JK-31 was not paralleled by elevated host cell adherence rates compared with the rates for Vomp-negative B. quintana strains. Our results suggest that the Vomps play a leading role in the angiogenic reprogramming of host cells by B. quintana but not in the adherence to host cells.
External Publication Status:published
Document Type:Article
Affiliations:MPI für Entwicklungsbiologie
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