Uma Nagarajan, PhD

Uma Nagarajan, PhD

Assistant Professor
8312B Molecular Biology Research Bldg


Chlamydia trachomatis is the most common sexually transmitted bacterial pathogen that causes Fallopian tube inflammation and subsequent tubal infertility in women.  Currently, more than 2 million young adults are infected and the annual cost of complications exceeds 2 billion dollars, making Chlamydia infection a huge public health problem. Chlamydia spp. are obligate intracellular pathogens that replicate inside an inclusion within infected cells. A Th1-dependent adaptive immune response is required for effective eradication of chlamydial infection. Primarily, an innate immune response to infection involves up regulation of a wide assortment of genes, including proinflammatory cytokines such as TNFa, IFN-b, IL-1b and IL-6, by the infected cells. which contribute to the development of oviduct pathology in the mouse model. The research in my laboratory is mainly focused to understand the innate immune responses to chlamydial infection and its role in genital tract pathology. Specifically, we are interested in delineating pathogen recognition by the host, signaling pathways that lead to the induction of innate immune cytokines in vitro and their downstream cellular effects in vitro and vivo. The current projects in the laboratory are examining the mechanisms of type I IFN and IL-1 induction during Chlamydia infection, with the overall hypothesis that cell death pathways driven by these cytokines result in a cascade of inflammatory events resulting in tissue damage. We also work in close collaboration with Dr. Toni Darville, Dr. Catherine O Connell and Dr. XiongJing Zheng, in the Infectious disease Division to form a collaborative “UNC Chlamydia group”, to understand chlamydial pathogenesis and translate the findings in the mouse model to human disease.


Zhang Y, Yeruva L, Marinov A, Danciu, T, Rank, RG, Wyrick PB, Lupashin V and Nagarajan UM. The DNA sensor - cyclic GMP-AMP synthase (cGAS) is essential for induction of IFN beta during Chlamydia trachomatis infection. J Immunol. 2014. 193:2394-2404 (Featured In this Issue p2039) PubMed PMID: 25070851

Frazer LC, Sullivan JE, Zurenski MA, Mintus M, Tomasak TE, Prantner D, Nagarajan UM, Darville T. CD4+ T cell expression of MyD88 is essential for normal resolution of Chlamydia muridarum genital tract infection. J Immunol. 2013 Oct 15;191(8):4269-79. PubMed PMID: 24038087

Pokrovskaya ID, Szwedo JW, Goodwin A, Lupashina TV, Nagarajan UM, Lupashin VV.  Chlamydia trachomatis hijacks intra-Golgi COG complex-dependent vesicle trafficking pathway. Cell Microbiol. 2012 May; 14(5):656-68. PubMed PMID: 22233276

Nagarajan UM, Sikes JD, Yeruva L, Prantner D. Significant role of IL-1 signaling, but limited role of inflammasome activation, in oviduct pathology during Chlamydia muridarum genital infection. J Immunol. 2012 Mar 15; 188(6):2866-75. PubMed PMID:  22331066

Prantner D, Sikes JD, Hennings L, Savenka AV, Basnakian AG, Nagarajan UM. Interferon regulatory transcription factor 3 protects mice from uterine horn pathology during Chlamydia muridarum genital infection. Infection and Immunity. 2011 Oct; 79(10):3922-33. PubMed PMID: 21788382

Prantner D, Darville T, Nagarajan UM*. Stimulator of IFN gene is critical for induction of IFN-beta during Chlamydia muridarum infection. J Immunol. 2010 Mar 1; 184(5):2551-60. PubMed PMID: 20107183

Complete list of publications


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