Evidence of a leading role for VEGF in Bartonella henselae-induced endothelial cell proliferations
Article first published online: 20 DEC 2001
Volume 3, Issue 9, pages 623–632, September 2001
How to Cite
Kempf, V. A. J., Volkmann, B., Schaller, M., Sander, C. A., Alitalo, K., Rieß, T. and Autenrieth, I. B. (2001), Evidence of a leading role for VEGF in Bartonella henselae-induced endothelial cell proliferations. Cellular Microbiology, 3: 623–632. doi: 10.1046/j.1462-5822.2001.00144.x
- Issue published online: 20 DEC 2001
- Article first published online: 20 DEC 2001
- Received 20 April, 2001; revised 25 June, 2001; accepted 29 June, 2001.
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.