Unraveling the molecular events in the lung innate immune response to tuberculosis
Larry Schlesinger (Center for Microbial Interface Biology, The Ohio State University)
(January 4, 2010 2:30 PM - 3:30 PM)
Tuberculosis continues to cause the suffering and death of millions of people in the world each year. Growing numbers of multi drug- and extensively drug-resistant bacterial strains are contributing to the problem as well as coincident HIV infection and a vaccine with variable efficacy. New therapies and vaccines require a more complete and integrated knowledge of the host immune response to infection. During infection, M. tuberculosis bacilli traverse the lung airways and settle in the alveolar spaces where they encounter alveolar macrophages (AMF). The alveolus is a highly immune-regulated microenvironment and AMF contribute to this by displaying an anti-inflammatory phenotype also known as an "alternative activation state". This biological state allows AMF to effectively clear microbes and particles within the alveolus while minimizing collateral inflammatory damage, but on the other hand may be exploited by the host-adapted M. tuberculosis. Our ongoing studies are characterizing the unique interactions that occur between M. tuberculosis, macrophages and components of the innate immune system during lung infection, including aspects related to host susceptibility. Examples of the scientific platforms being used will be highlighted during this seminar.