Lalita Ramakrishnan, M.B.B.S., Ph.D.
Associate Professor, Microbiology and
Adjunct Associate Professor, Immunology

Department of Microbiology
University of Washington
Office K-443C HSC, Box 357242
1959 NE Pacific Street
Seattle, WA 98195-7650
Tel: 206.616-4286
Fax: 206.616-1575
Email: lalitar@u.washington.edu

Ramakrishnan Lab Members

Dr. Ramakrishnan received her M.B.B.S. in Vadodara, India in 1983 and her Ph.D. in Immunology at Tufts University, Boston in 1990. Prior to joining theUniversity of Washington in 2001, she did a medical residency at the Tufts-New England Medical Center in Boston, an infectious diseases fellowship at the University of California San Francisco and a post doctoral fellowship at Stanford University. Her research is funded by the National Institutes of Health, the Burroughs Wellcome Foundation and the Akibene Foundation.

We are interested in understanding the pathogenesis of tuberculosis. Tuberculous infection results in the formation of granulomas, complex immune structures that are composed of differentiated macrophages, lymphocytes and other immune cells. However, bacteria can persist within granulomas despite the development of antigen-specific immunity. We are trying to understand the mechanistic basis of mycobacterial persistence, the mechanisms of granuloma formation and its role in tuberculosis. We have developed the zebrafish as model to study immunity to tuberculosis. Zebrafish are naturally susceptible to tuberculosis caused by Mycobacterium marinum, a close genetic relative of M. tuberculosis, the agent of human tuberculosis. We exploit the optical transparency and genetic tractability of the zebrafish to monitor the infection process in real-time and modulate it using genetically defined host and bacterial mutants. Our research is focused on identifying determinants of host susceptibility and resistance to tuberculosis using a forward genetic screen. Our goal is to understand how bacterial and host immune determinants interface to result in persistent infection. Our research should shed light on tuberculosis pathogenesis as well as fundamental mechanisms of immune cell chemotaxis, adhesion and aggregation as well as immune regulation.

Students currently training in the Ramakrishnan Lab: Kristin Adams, Russell Berg, Sachi Seilie

Recent publications:

M. Brannon, J. M. Davis, C. Hall, P. Crozier, J. R. Mathias, A. Huttenlocher, L. Ramakrishnan* and S.  Moskowitz*. 2009. Pseudomonas aeruginosa Type III secretion system interacts with phagocytes to modulate systemic infection of zebrafish embryos.  Cell Microbiol, 11:755-768

J.M. Davis and L. Ramakrishnan.  2009.  The role of the granuloma in the expansion and dissemination of  early tuberculous infection.  Cell 136:37-49

C.L. Cosma, O. Humbert, D.R. Sherman. L. Ramakrishnan. 2008. Trafficking of Superinfecting Mycobacterium into Established Granulomas Occurs in Mammals and is Independent of the Mycobacterial Erp and ESX-1/RD1 Virulence Loci. J Infect Dis, 198:1851-5

H. Clay, HE Volkman and L. Ramakrishnan. 2008.  TNF signaling mediates resistance to mycobacteria by inhibiting bacterial growth and macrophage death but is not required for tuberculous granuloma formation. Immunity 29:283-294.

H. Clay, J.M. Davis, D. Beery, A. Huttenlocher, S. E.Lyons and L. Ramakrishnan. 2007. Dichotomous role of the macrophage in earlyMycobacteriummarinuminfection of thezebrafish.Cell Host and Microbe2:29-39.

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Updated 8/24/09