Murugesan Rajaram, PhD

About

Biography

The central goal of our research program is to understand the molecular mechanism of host response to microbial infections of humans, particularly bacterial and viral diseases, using animal and in vitro models. Our research has focused on two major areas:

1. Understand the molecular mechanism and pathogenesis of cardiac dysfunction caused by pneumonia causing bacterial and viral infectious agents. In particular, we are interested in studying the cardiac immune cell (macrophages) phenotypes, and their role in both steady state heart function and during infection (Pseudomonas aeruginosa, Influenza Flu and non-tuberculosis mycobacterium species). Recently, cardiac macrophages emerged as an important regulator of cardiac inflammation (during infection and sterile inflammation), cardiac fibrosis and tissue repair. In addition to their routine immune surveillance function, cardiac macrophages are critical for cardiac electrical conduction. Our laboratory is interested in studying the source, phenotype and function of these cardiac macrophages and other immune cells in the heart during infection. Additionally, our studies focus on understanding how aging mediated immune dysregulation influences cardiac immune cell phenotype and immune function during infection (both heart and lungs).
2. Define the mechanism of Mycobacterium tuberculosis drug resistance. Tuberculosis, a lung disease caused by Mycobacterium tuberculosis (M.tb), kills nearly 2 million people annually. Tuberculosis (TB) treatment requires a combination of four or six anti-TB drugs for at least six months, and the adherence of long term multidrug treatment is often difficult and mismanaged, which leads to the development of drug resistant M.tb. Global prospects for TB control are challenged by the emergence of drug resistant strains, especially those that are multidrug resistant (MDR-TB) and extensively drug resistant (XDR-TB). Our laboratory aims to understand the intricate interplay between mycobacteria and their host response. By identifying key mechanisms and pathways utilized by M.tb to hijack the host immune system, we hope to find ways to shorten the TB treatment regimen. On this line, we recently discovered that M.tb drives host cells to become drug resistant by increasing the expression of the drug efflux pump (MDR1) before it develops drug resistance. Currently, we are taking a genetic approach to identify the M.tb mutation under low antibiotic conditions. Also, we are testing whether an MDR-1 inhibitor (currently in clinical trial in the cancer field) reduces TB burden in mice.

Credentials

Research

News and media

My news coverage

• Genetic Mutation Linked to Flu-related Heart Complications in Mice