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5 - Bartonella signaling and endothelial cell proliferation
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- By Garret Ihler, Department of Medical Biochemistry and Genetics, Texas A&M College of Medicine, Anita Verma, Laboratory of Respiratory and Special Pathogens, DBPAP/CBER, Food and Drug Administration, Javier Arevalo, Proctor and Gamble America Latina
- Edited by Alistair J. Lax, King's College London
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- Book:
- Bacterial Protein Toxins
- Published online:
- 15 September 2009
- Print publication:
- 10 January 2005, pp 81-116
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- Chapter
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Summary
Bartonella bacilliformis is the causative agent of Carrion's disease (for a recent medical review, see Maguina and Gotuzzo, 2000). B. bacilliformis was in a genus by itself until recent taxonomic revisions associated it with other bacteria. Now there are sixteen known species of Bartonella, of which seven are associated with human disease. B. bacilliformis enters the bloodstream of humans through the bite of an insect vector and targets primarily erythrocytes and endothelial cells.
For many years, it seemed as though important and interesting conclusions about the mechanism of angiogenesis might result from the study of B. bacilliformis, which can initiate and perpetuate lesions formed of proliferating endothelial cells and newly formed capillaries. Since then, the Science juggernaut has moved on, more rapidly for angiogenesis than for Bartonella, and so it now appears that we can best understand B. bacilliformis (and the closely related Bartonella henselae) by reference to the known biology of angiogenesis. However, study of B. bacilliformis has made at least one useful contribution to our knowledge of angiogenesis. Entry of B. bacilliformis by vacuole formation and macropinocytosis was shown to be accomplished by activation of Rho, Rac, and Cdc42 GTPases. This process appeared to be analogous to the angiogenic process by which endothelial cells take in large volumes of extracellular fluids to form large central vacuoles, which perhaps fuse between cells to form the nascent capillary.