Science for Health
14 November 2012
Two new programme leaders track who joined the Institute in 2012 describe their new research programmes.
Veni Papayannopoulos and Max Gutierrez joined NIMR this year to set up new research programmes in infections and immunity, working on neutrophils and Mycobacterium tuberculosis, respectively.
Veni was born in Greece. He studied Biochemistry and Molecular Biology at Rutgers University (1998), where he worked with Ken Irvine on Drosophila development, and then in 2004 gained his PhD in Biochemistry from UCSF working with Wendell Lim on the regulation of actin dynamics. Subsequently he worked as a postdoc at the Max Planck Institute for Infection Biology, Berlin with Arturo Zychlinsky studying the formation of neutrophil extracellular traps.
Neutrophils are an essential part of the immune system. These phagocytes can fight infections extracellularly by releasing neutrophil extracellular traps (NETs) - web like structures made up of strands of chromatin, which are decorated with antimicrobial factors and can trap and kill a variety of pathogens. NETs are also suspected to trigger autoimmune disease and have been found in the vasculature during sepsis and thrombosis where they can interfere with blood flow and damage the cells that line up the blood vessels.
We are using human neutrophils and mouse models to understand the molecular mechanisms that drive NET release and NET function during infection and disease. We are also investigating neutrophil priming and the interplay of neutrophils with other cells of the immune system.
Max was born in Argentina. He studied biochemistry and molecular biology at the University of San Luis, gaining his PhD in 2005 studying the role of autophagy in infection. After three years as a postdoctoral scientist working in mycobacterial phagosome dynamics in Gareth Griffiths’ lab at EMBL, Heidelberg, he moved to the Helmholtz Centre for Infection Research in Braunschweig, Germany as a head of a research group in phagosome biology.
Phagocytes, cells able to eat foreign particles, are a critical part of the immune defense. Phagocytosis is the process by which phagocytes ingest relatively big particles including microbes. The resulting intracellular vacuoles, termed phagosomes, undergo dynamic events that modify their contents and change the environment into a ‘microbial hell’. The extremely harsh conditions within the phagosome are central to its microbicidal function, representing the first line of defense against infection.
Certain pathogens such as Mycobacterium tuberculosis are able to convert the phagosome into a good place to live within eukaryotic cells. In fact, the key event during M. tuberculosis infection is the ability of this pathogen to survive within phagosomes in host cells. Living within phagocytes represents an advantage in many aspects, so intracellular bacteria somehow adapt to this long-term phagosome lifestyle and live within the cells.
The aim of my research is to give insights into a) the molecular mechanisms whereby M. tuberculosis manipulates the phagosomal environment and avoids killing by phagocytes and b) how host phagocytes eliminate mycobacteria. This is important to find possible therapeutic strategies that enhance this natural response.
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