The Bartonella autotransporter BafA activates the host VEGF pathway to drive angiogenesis

Kentaro Tsukamoto (), Naoaki Shinzawa, Akito Kawai, Masahiro Suzuki, Hiroyasu Kidoya, Nobuyuki Takakura, Hisateru Yamaguchi, Toshiki Kameyama, Hidehito Inagaki, Hiroki Kurahashi, Yasuhiko Horiguchi and Yohei Doi ()
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Kentaro Tsukamoto: Fujita Health University School of Medicine
Naoaki Shinzawa: Osaka University
Akito Kawai: Fujita Health University School of Medicine
Masahiro Suzuki: Fujita Health University School of Medicine
Hiroyasu Kidoya: Osaka University
Nobuyuki Takakura: Osaka University
Hisateru Yamaguchi: Fujita Health University
Toshiki Kameyama: Fujita Health University
Hidehito Inagaki: Fujita Health University
Hiroki Kurahashi: Fujita Health University
Yasuhiko Horiguchi: Osaka University
Yohei Doi: Fujita Health University School of Medicine

Nature Communications, 2020, vol. 11, issue 1, 1-14

Abstract: Abstract Pathogenic bacteria of the genus Bartonella can induce vasoproliferative lesions during infection. The underlying mechanisms are unclear, but involve secretion of an unidentified mitogenic factor. Here, we use functional transposon-mutant screening in Bartonella henselae to identify such factor as a pro-angiogenic autotransporter, called BafA. The passenger domain of BafA induces cell proliferation, tube formation and sprouting of microvessels, and drives angiogenesis in mice. BafA interacts with vascular endothelial growth factor (VEGF) receptor-2 and activates the downstream signaling pathway, suggesting that BafA functions as a VEGF analog. A BafA homolog from a related pathogen, Bartonella quintana, is also functional. Our work unveils the mechanistic basis of vasoproliferative lesions observed in bartonellosis, and we propose BafA as a key pathogenic factor contributing to bacterial spread and host adaptation.

Date: 2020
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DOI: 10.1038/s41467-020-17391-2

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