The autotransporter BafA contributes to the proangiogenic potential of Bartonella elizabethae.


Journal

Microbiology and immunology
ISSN: 1348-0421
Titre abrégé: Microbiol Immunol
Pays: Australia
ID NLM: 7703966

Informations de publication

Date de publication:
May 2023
Historique:
revised: 14 02 2023
received: 14 01 2023
accepted: 19 02 2023
medline: 4 5 2023
pubmed: 23 2 2023
entrez: 22 2 2023
Statut: ppublish

Résumé

Bartonella elizabethae is a rat-borne zoonotic bacterium that causes human infectious endocarditis or neuroretinitis. Recently, a case of bacillary angiomatosis (BA) resulting from this organism was reported, leading to speculation that B. elizabethae may also trigger vasoproliferation. However, there are no reports of B. elizabethae promoting human vascular endothelial cell (EC) proliferation or angiogenesis, and to date, the effects of this bacterium on ECs are unknown. We recently identified a proangiogenic autotransporter, BafA, secreted from B. henselae and B. quintana, which are recognized as Bartonella spp. responsible for BA in humans. Here, we hypothesized that B. elizabethae also harbored a functional bafA gene and examined the proangiogenic activity of recombinant B. elizabethae-derived BafA. The bafA gene of B. elizabethae, which was found to share a 51.1% amino acid sequence identity with BafA of B. henselae and 52.5% with that of B. quintana in the passenger domain, was located in a syntenic region of the genome. The recombinant protein of the N-terminal passenger domain of B. elizabethae-BafA facilitated EC proliferation and capillary structure formation. Furthermore, it upregulated the receptor signaling pathway of vascular endothelial growth factor, as observed in B. henselae-BafA. Taken together, B. elizabethae-derived BafA stimulates human EC proliferation and may contribute to the proangiogenic potential of this bacterium. So far, functional bafA genes have been found in all BA-causing Bartonella spp., supporting the key role BafA may play in BA pathogenesis.

Identifiants

pubmed: 36810719
doi: 10.1111/1348-0421.13057
doi:

Substances chimiques

Type V Secretion Systems 0
Vascular Endothelial Growth Factor A 0

Types de publication

Case Reports Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

248-257

Subventions

Organisme : Ohyama Health Foundation
Organisme : Japan Society for the Promotion of Science
ID : KAKENHI [JP19K07548]
Organisme : Japan Society for the Promotion of Science
ID : [JP22K070602]
Organisme : Ichiro Kanehara Foundation
Organisme : Institute for Fermentation, Osaka
ID : G-2021-3-031
Organisme : Japan Agency for Medical Research and Development
ID : JP21lm0203005

Informations de copyright

© 2023 The Societies and John Wiley & Sons Australia, Ltd.

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Auteurs

Natsumi Suzuki (N)

Department of Microbiology, Fujita Health University School of Medicine, Toyoake, Japan.

Kayo Kumadaki (K)

Department of Microbiology, Fujita Health University School of Medicine, Toyoake, Japan.

Kaoru Tatematsu (K)

Department of Microbiology, Fujita Health University School of Medicine, Toyoake, Japan.

Yohei Doi (Y)

Department of Microbiology, Fujita Health University School of Medicine, Toyoake, Japan.
Department of Infectious Diseases, Fujita Health University School of Medicine, Toyoake, Japan.
Division of Infectious Diseases, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.

Kentaro Tsukamoto (K)

Department of Microbiology, Fujita Health University School of Medicine, Toyoake, Japan.

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