Interception of host angiogenic signalling limits mycobacterial growth

Stefan H. Oehlers, Mark R. Cronan, Ninecia R. Scott, Monica I. Thomas, Kazuhide S. Okuda, Eric M. Walton, Rebecca W. Beerman, Philip S. Crosier and David M. Tobin ()
Additional contact information
Stefan H. Oehlers: Center for Microbial Pathogenesis, Duke University Medical Center
Mark R. Cronan: Center for Microbial Pathogenesis, Duke University Medical Center
Ninecia R. Scott: Center for Microbial Pathogenesis, Duke University Medical Center
Monica I. Thomas: Center for Microbial Pathogenesis, Duke University Medical Center
Kazuhide S. Okuda: The University of Auckland, Auckland 1023, New Zealand
Eric M. Walton: Center for Microbial Pathogenesis, Duke University Medical Center
Rebecca W. Beerman: Center for Microbial Pathogenesis, Duke University Medical Center
Philip S. Crosier: The University of Auckland, Auckland 1023, New Zealand
David M. Tobin: Center for Microbial Pathogenesis, Duke University Medical Center

Nature, 2015, vol. 517, issue 7536, 612-615

Abstract: Using a model of tuberculosis in zebrafish, granuloma formation is shown to coincide with hypoxia and angiogenesis; furthermore, the pharmacological inhibition of the pro-angiogenic VEGF pathway reduces infection burden, suggesting a possible treatment strategy in patients with the disease.

Date: 2015
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DOI: 10.1038/nature13967

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