Rita Das, MD

Postdoctoral Fellow
Internal Medicine (Infectious Diseases)

Thesis Advisory

Richard Bucala

Thesis Project

Role of MIF in tuberculosis pathogenesis

MIF, macrophage migration inhibitory factor, is cytokine which causes “migration arrest” of macrophages in inflammatory lesions. It has been shown to have varying role in models of response to infection with different pathogens. It has a proposed deleterious effect in LPS-mediated endotoxemia - MIF knockout mice are protected from death and higher MIF levels are present in patients with septic shock. It has been shown to be indispensable, however, for immune control of intracellular pathogens, ie. Salmonella and Leishmania.

The focus of Dr. Das’ project is that MIF, which is a key mediator of the inflammatory process, plays an important role in the pathogenesis of tuberculosis disease. She anticipates that higher levels of MIF will be protective against tuberculosis infection, or mitigate the severity of disease. In vitro studies of MIF response to tuberculosis surface glycolipids in, monocyte/macrophage cell lines, murine bone marrow derived macrophages and human peripheral blood monocytes will be performed and in vivo studies of tuberculosis infection in wild type and MIF knock out mice. Finally, there are known polymorphisms in the promoter region of the MIF gene which create high and low producers of MIF in the populations. Apopulation genetics studies of MIF polymorphisms in tuberculosis infected patients will be performed to determine whether low producers of MIF are more susceptible to tuberculosis disease