
Evidence of a leading role for VEGF in Bartonella henselae ‐induced endothelial cell proliferations
Author(s) -
Kempf Volkhard A. J.,
Volkmann Bettina,
Schaller Martin,
Sander Christian A.,
Alitalo Kari,
Rieß Tanja,
Autenrieth Ingo B.
Publication year - 2001
Publication title -
cellular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.542
H-Index - 138
eISSN - 1462-5822
pISSN - 1462-5814
DOI - 10.1046/j.1462-5822.2001.00144.x
Subject(s) - bacillary angiomatosis , bartonella henselae , biology , vascular endothelial growth factor , angiogenesis , cancer research , immunology , vegf receptors , serology , antibody
Bartonella henselae causes the vasculoproliferative disorders bacillary angiomatosis (BA) and bacillary peliosis (BP). The pathomechanisms of these tumorous proliferations are unknown. Our results suggest a novel bacterial two‐step pathogenicity strategy, in which the pathogen triggers growth factor production for subsequent proliferation of its own host cells. In fact, B. henselae induces host cell production of the angiogenic factor vascular endothelial growth factor (VEGF), leading to proliferation of endothelial cells. The presence of B. henselae pili was associated with host cell VEGF production, as a Pil − mutant of B. henselae was unable to induce VEGF production. In turn, VEGF‐stimulated endothelial cells promoted the growth of B. henselae . Immunohistochemistry for VEGF in specimens from patients with BA or BP revealed increased VEGF expression in vivo . These findings suggest a novel bacteria‐dependent mechanism of tumour growth.