The Bartonella autotransporter BafA activates the host VEGF pathway to drive angiogenesis.
Level 5 - mechanism / opinion, no new human data
Preclinical in vitro and animal mechanistic study without human clinical data
PubMed 32678094 · doi:10.1038/s41467-020-17391-2
What was done
Researchers used functional transposon-mutant screening in Bartonella henselae to identify the bacterial mitogenic factor driving host vasoproliferative lesions. They evaluated the identified autotransporter, BafA, examining the effects of its passenger domain on endothelial cell proliferation, tube formation, microvessel sprouting, and angiogenesis in mice, while testing for interaction with VEGF receptor-2 and activity of a Bartonella quintana homolog.
What was found
No quantitative values or effect sizes are reported in the abstract. The screen identified BafA as a pro-angiogenic autotransporter whose passenger domain stimulated cell proliferation, tube formation, microvessel sprouting, and mouse angiogenesis. BafA interacted with VEGFR2 to activate downstream signaling as a VEGF analog, and the B. quintana homolog displayed similar activity.
Why it matters
These findings uncover a mechanism of bacterial pathogenesis in bartonellosis, demonstrating that a bacterial factor can directly mimic host VEGF to drive angiogenesis and facilitate host adaptation.
Limits
The study is restricted to in vitro and mouse models with no human clinical testing. Quantitative data, sample sizes, and effect magnitudes are not reported in the abstract.
Cited by
- supports Elevated VEGF levels occur in Long COVID, Bartonella infections, and cancer.
- context Bartonella infection induces vascular endothelial growth factor (VEGF) elevation in long COVID patients.