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Abstract

Mycobacterium tuberculosis causes widespread, persistent infection, often residing in macrophages that neither sterilize the bacilli nor allow them to cause disease. How macrophages restrict growth of pathogens is one of many aspects of human phagocyte biology whose study relies largely on macrophages differentiated from monocytes in vitro . However, such cells fail to recapitulate the phenotype of tissue macrophages in key respects, including that they support early, extensive replication of M. tuberculosis and die in several days. Here we found that human macrophages could survive infection, kill Mycobacterium bovis BCG, and severely limit the replication of M. tuberculosis for several weeks if differentiated in 40% human plasma under 5%�10% (physiologic)oxygen in the presence of GM-CSF and/or TNF-�± followed by IFN-�³. Control was lost with fetal bovine serum, 20% oxygen, M-CSF, higher concentrations of cytokines, or premature exposure to IFN-�³. We believe that the new culture method will enable inquiries into the antimicrobial mechanisms of human macrophages.

Biography

Guillaume Vogt was born in France, in 1977. He received a Ph.D. degree from the University Paris Ren? Descartes, Necker-Enfants Malades Medical School, Paris, France, in 2007. From 2007 to 2010, he worked as postdoctoral associate in Weill Medical College of Cornell University, New York, USA. In 2010, he joined the Rockefeller University, New York, USA, as part of the St. Giles Laboratory of Human Genetics of Infectious Diseases directed by Pr. Jean-Laurent Casanova. Among various distinctions, he received the distinguished Thermo (Electron Corporation) Prize (formerly Jouan Prize) in Biotherapy, and the Prize of Pediatric Pathology, Association for Study of Pediatric Pathology, Paris, France. He reviewed papers for high-ranking journals and is currently editor of the journal ?Case Reports in Genetics?. He currently attends to describe the first genetic etiology of Whipple?s Disease. Nevertheless, he is mainly interested in genetics, infectious disease, chemical therapy and forensic genetic