University of California, Riverside

School of Medicine



Faculty Biographies


Meera G. Nair

Assistant Professor of Biomedical Sciences

Meera Nair

University of California, Riverside
Riverside, CA 92521

Tel: (951) 827-7734
E-mail: meera.nair@ucr.edu
Office: 301 School of Medicine Research Building

Education and Training

  • B.Sc. (Honors), Imperial College London, United Kingdom, 1999
  • Ph.D., University of Edinburgh, United Kingdom, 2004
  • Postdoctorate, University of Pennsylvania, Philadelphia, 2011

Research Summary

Research in my lab is focused on understanding how the optimal host immune response to mucosal pathogens is generated. This research may have significant impact on public health as infections of the mucosa are prevalent and debilitating for the following reasons; first, mucosal sites are continually exposed to the external environment and invasive pathogens and second, they cause severe, sometimes lethal, consequences for the host. My lab investigates infections of the lung and the gastrointestinal tract, which are especially debilitating because these organs provide essential physiologic functions for the host including oxygen and nutrition uptake respectively. We utilize mouse in vivo infection models to address two main questions; (i) how do macrophages contribute to mucosal immunity and inflammation and (ii) what is the functional significance of Resistin-Like Molecules (RELM) in these infection models?

(i) Macrophages in mucosal immunity and inflammation

In order to understand the biology and function of macrophages in infectious and non-infectious inflammation, I have spent over 15 years establishing murine models of mucosal inflammation, including: bleomycin-induced lung fibrosis, helminth infection, and Citrobacter and dextran sodium sulfate induced colitis. In particular, we have focused on the function of alternatively activated macrophages (AAMac) that are dominant cell-types in helminth infection, tissue injury and chronic allergic inflammation. Using these models, we have identified specific functions for AAMac-derived proteins in regulating innate and adaptive inflammatory responses. Targeting these pathways may provide new therapeutic strategies for treatment of mucosal diseases. For this we are using multiple macrophage reporter mice to track macrophage recruitment and behavior in the inflamed tissue, as well as mouse models with genetic deficiencies in macrophage recruitment or macrophage-derived proteins.


(ii) The biology of RELM proteins

We are currently investigating the molecular and cellular mechanism by which RELM proteins influence mucosal immunity. We have shown that RELMa and RELMb are potently induced in multiple mucosal infections, including murine hookworm infection of the lung and intestine, as well as bacterial infection of the colon. We also use humanized transgenic mice and clinical samples from helminth-infected patients to investigate the function of the human RELM protein ‘resistin’. Understanding the immunologic basis of RELM protein function may provide new cellular and molecular targets to treat infection-induced inflammation or promote immunity to helminth and bacterial pathogens.

Selected Publications

  • Nair M.G., Herbert R.H. Immune polarization by hookworms: taking cues from T helper type 2, type 2 innate lymphoid cells and alternatively activated macrophages. Immunology 2016
  • Bennett K.M., Parnell E.A., Sanscartier C., Parks S., Chen G., Nair M.G., Lo D.D. Induction of Colonic M Cells during Intestinal Inflammation. Am J Pathol. 2016
  • Chen G., Wang S.H., Jang J.C., Odegaard J.I., Nair M.G. Comparison of RELMα and RELMβ Single- and Double-Gene-Deficient Mice Reveals that RELMα Expression Dictates Inflammation and Worm Expulsion in Hookworm Infection. Infect Immun. 2016 - UCR Today article
  • Kirk S. B. Bergstrom ,Vijay Morampudi,Justin M. Chan, Ganive Bhinder, Jennifer Lau, Hyungjun Yang, Caixia Ma, Tina Huang, Natasha Ryz, Ho Pan Sham, Maryam Zarepour, Colby Zaph, David Artis, Meera Nair, Bruce A. Vallance. Goblet Cell Derived RELM-β Recruits CD4+ T Cells during Infectious Colitis to Promote Protective Intestinal Epithelial Cell Proliferation. PLoS Pathogens. 2015.
  • Barnes M.A., Carson M.J., Nair M.G. How catecholamines and adipokines influence macrophages in immunity, metabolism and the central nervous system. Cytokine. 2015.
  • Jang J.C., Chen G., Wang S.H., Chung J.I., Camberis M., Le Gros G., Cooper P.J., Steel C., Nutman T.B., Lazar M.A., Nair M.G. Human resistin is induced in multiple helminth infections and promotes inflammatory monocytes and increased parasite burden. PLoS Pathogens. 2015. - UCR Today article
  • Chen G., Chan A.J., Chung J.I., Jang J.C., Osborne L.C., Nair M.G. Polarizing the T helper 17 response in Citrobacter rodentium infection via expression of RELM-α. Gut microbes. 2014
  • Jang J.C. and Nair M.G. Alternatively Activated Macrophages Revisited: New Insights into the Regulation of Immunity, Inflammation and Metabolic Function following Parasite Infection. Current Immunology Reviews. 2014.
  • Osborne L., Joyce K.L., Alenghat T., Giacomin P.R., Sonnenberg G.F., Du Y., Bergstrom K., Vallance B., Nair M.G. Resistin-like molecule (RELM) α promotes Th17 cell responses and bacterial-induced colitis. Journal of Immunology. 2013.
  • Joyce K.L., Morgan W., Artis D., Greenberg R., Nair M.G. Using eggs from Schistosoma mansoni as an in vivo model of helminth-induced lung inflammation. Journal of Visualized Experiments. 2012.
  • Nair M.G., Du, Y., Perrigoue J.G., Zaph C., Taylor J.J., Goldschmidt M., Swain G.P., Yancopoulos G.D., Valenzuela D.M., Murphy A., Karow M., Stevens S., Pearce E.J., Artis D. Alternatively activated macrophage-derived RELM-α is a negative regulator of type 2 inflammation in the lung. Journal of Experimental Medicine 4:937-52. 2009.

More Information 

General Campus Information

University of California, Riverside
900 University Ave.
Riverside, CA 92521
Tel: (951) 827-1012

School Information

School of Medicine
2608 School of Medicine Education Building

Admissions Inquiries: (951) 827-7353
E-mail: medadmissions@ucr.edu

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