Gopinath Venugopal, PhD

Research Assistant Professor

B.S. Biochemistry University of Madras, Chennai, India
M.S. Biochemistry University of Madras, Chennai, India
Ph.D. Biomedical Sciences, Institute of Immunology, Free University Berlin, Germany
Postdoc, Dept. of Microbiology and Immunology, University of Arkansas for Medical Sciences, AR, USA

Phone: 252-744-3132
Fax:  252-744-3104
E-MAIL: venugopalg24@ecu.edu

Yersinia pestis, a NIAID Category A priority bacterial pathogen is responsible for causing bubonic, septicemic, and pneumonic plague. The most severe manifestation of plague is pneumonic plague, which results in disease that is 100% lethal without treatment. Primary pneumonic plague results from inhalation of respiratory droplets contaminated with Y. pestis and has the potential to be used as a bioweapon due to its lethality and transmissibility in aerosolized form and it can re-emerge as a threat around the globe at any time. Pneumonic plague is characterized by its biphasic progression of disease, which includes an initial pre-inflammatory phase followed by the abrupt onset of a proinflammatory phase in the lungs. The lethality of pneumonic plague is largely attributed to the abrupt onset of a severe and lethal host inflammatory response defined by a pro-inflammatory cytokine storm and the massive infiltration of neutrophils into the pulmonary compartment.

I work closely with Dr. Pechous to study and characterize the host/pathogen interactions and factors responsible for the biphasic progression of pneumonic plague. My primary interest is to understand and identify the bacterial and host factors that drive pulmonary inflammation, because Y. pestis effectively suppresses host immune responses early in the lung to establish infection. More specifically, I am trying to understand the role and contribution of yersinia outer proteins (Yops) on host inflammasome assembly and activation during very early stages of infection. Based on literature, we know Yop injection interferes with inflammasome activation, preventing secretion of IL-18 and IL-1β and modulating host cell death pathways by inhibiting pyroptosis. Of note, the work characterizing the impact of individual Yops on inflammasome activation has largely been performed using attenuated strains of Y. pestis or the enteric pathogen such as Y. pseudotuberculosis in cell culture models. Therefore, the focus of our lab is to understand how these findings translate to infection in the lung with fully virulent Y. pestis.  And in another project, I am studying the molecular mechanism involved and contribution of Y. pestis protein YbtX to the onset of host pro-inflammatory responses during pneumonic plague.

Selected Publications:

  • Venugopal G, and Pechous RD. Yersinia pestis and pneumonic plague: insight into how a lethal pathogen interfaces with innate immune populations in the pulmonary compartment to cause severe disease. Cellular Immunology (2024). https://pubmed.ncbi.nlm.nih.gov/39002222/
  • Venugopal G, Bird JT, Roys H, Bowlin A, Fry L, Byrum SD, Weinkopff T. Both the infection status and inflammatory microenvironment induce transcriptional remodeling in macrophages in murine leishmanial lesions. Journal of Parasitology (2023). https://pubmed.ncbi.nlm.nih.gov/37270767/
  • Venugopal G, Bird JT, Washam CL, Roys H, Bowlin A, Byrum SD, Weinkopff T. In vivo transcriptional analysis of mice infected with Leishmania major unveils cellular heterogeneity and altered transcriptomic profiling at single-cell resolution. PLOS Neglected Tropical Diseases (2022). https://pubmed.ncbi.nlm.nih.gov/35789215/
  • Bettadapura M, Roys H, Bowlin A, Venugopal G, Washam CL, Fry L, Murdock S, Wanjala H, Byrum SD, Weinkopff T. HIF-alpha activation impacts macrophage function during murine Leishmania major Pathogens (2021). https://pubmed.ncbi.nlm.nih.gov/34959539/
  • Bowlin A, Roys H, Wanjala H, Bettadapura M, Venugopal G, Surma J, Simon MS, Weinkopff T. Hypoxia-inducible factor signaling in macrophages promotes lymphangiogenesis in Leishmania major Infection and Immunity (2021). https://pubmed.ncbi.nlm.nih.gov/34031127/
  • Venugopal G, O’Regan NL, Babu S, Schumann RR, Srikantam A, Merle R, Hartmann S, Steinfelder S. Association of a PD-L2 gene polymorphism with chronic lymphatic filariasis in a South Indian Cohort. American Journal of Tropical Medicine and Hygiene (2019). https://www.ncbi.nlm.nih.gov/pubmed/30594267
  • Venugopal G, Mueller M, Hartmann S, Steinfelder S. Differential immunomodulation in human monocytes versus macrophages by filarial cystatin. PLOS ONE (2017). https://www.ncbi.nlm.nih.gov/pubmed/29141050
  • O’Regan NL, Steinfelder S, Venugopal G, Rao GB, Lucius R, Srikantam A, Hartmann S. Brugia malayi microfilariae induce a regulatory monocyte/macrophage phenotype that suppresses innate and adaptive immune responses. PLOS Neglected Tropical Diseases (2014). https://www.ncbi.nlm.nih.gov/pubmed/25275395
  • Kumar NP, Gopinath V, Sridhar R, Hanna LE, Banurekha VV, Jawahar MS, Nutman TB, Babu S. IL-10 dependent suppression of Type 1, Type 2 and Type 17 cytokines in active pulmonary tuberculosis. PLOS ONE (2013).https://www.ncbi.nlm.nih.gov/pubmed/23544075

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