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DepartmentMicrobiology, Immunology & Molecular Genetics
Dube, Peter H., Ph.D.
Dr. Dube has studied Yersinia pathogenesis for the last 15 years and he has developed a variety of unique tools to study interaction of Yersinia with intestinal epithelial cells in vitro and in vivo. Dr. Dube has been continuously grant funded in the area of Yersinia pathogenesis and host immune responses for more than 15 years during this time he has served on numerous governmental advisory boards in the ares of mucosal immunology and infectious disease.
Much of his work has evaluated host responses to Yersinia infection and regulation of gut inflammation and inflammation-associated sequellae induced after infection. Specifically, the Dube lab has elucidated the role of virulence factors produced by Yersinia in the modulation of signaling by IL-1 family members.
He brings extensive research experience in immunology, bacterial pathogenesis, and host-immune responses to this project. The current application is an extension of novel findings recently reported by the Dube lab describing the mechanism of IL-18 expression in intestinal epithelial cells following Yersinia infection.
Dr. Dube’s laboratory was the first to elucidate the mechanisms of integrin-mediated inflammasome activation in intestinal epithelial cells (Thinwa et al. 2014 J. Immunol.). These studies showed that a bacterial protein called invasin was capable of providing the first signal for NLRP3-dependent IL-18-mediated protective responses. The current application exploits and applies these findings and the novel reagents developed by the Dube lab to the treatment and prevention of inflammatory bowel disease and colorectal cancer.
Dr. Dube has made significant efforts to improve the training environment for graduate students and fellows over the last 7 years. He has lead the Microbiology, Immunology & Molecular Genetics training track at UT Health San Antonio and has been instrumental in the last two redesigns of the graduate school curricula. Part of his efforts have been to enhance exposure of students to learning approaches to graduate education.
Ph.D., Biochemistry at the State University of New York at Stony Brook
The research in Dr. Peter Dube’s lab is focused on inflammation and how inflammation leads to disease. In particular, we investigate how viral and bacterial pathogens and their products influence inflammatory responses. The major research interests are acute infections of the lungs by viral and bacterial pathogens as well as co-infections, pulmonary infections leading to asthma or the exacerbation of asthma, infectious gastroenteritis caused by invasive bacterial pathogens and vaccine development.
Dr. Dube and his team have extensive experience working with highly pathogenic organisms at BSL-3 and ABSL-3. Dr. Dube directs the Select Agent Research Core which provides facilitates research with SARS-CoV-2 at BSL-3/ABSL-3. The Dube laboratory has several active research programs investigating the pathogenesis of the SARS-CoV-2 virus, the causative agent of COVID-19. We are interested in the pathogenesis of the SARS-CoV-2 virus and the related coronaviruses SARS-CoV and MERS-CoV. We are also investigating the role of co-infections in severe COVID-19 disease. The laboratory is testing several novel vaccine platforms for the prevention of SARS-CoV-2 , SARS, and MERS infection.
We have research interests in T-cell-mediated vaccines for the prevention and treatment of malignancies and infectious diseases. We have applied our Listeria-based vaccines for the prevention of melanoma and Yersinia infections. We are applying this platform to the development of beta-coronavirus vaccines and therapeutic melanoma vaccines.
Our interests in asthma revolve around Mycoplasma pneumoniae and a toxin produced by this pathogen called the Community Acquired Respiratory Distress Syndrome toxin (CARDS toxin). Mycoplasma pneumoniae is often associated with acute exacerbations of asthma in children and adults and recent data suggests that CARDS toxin might be linked to a subset of asthma exacerbations.
Awards & Accomplishments
|2004||ERC New Faculty Award UT Health San Antonio “Host Responses to Yersinia Pestis”|
|2003||Howard Hughes Medical Institute Young Investigator Award|
|2000||Keck Postdoctoral Fellowship Award, Washington University School of Medicine|
- American Society For Microbiology
- American Association of Immunologists
- Editorial board member for Infection and Immunity
- Frontiers in Cellular Microbiology
Evseev AI, Semenov I, Archer CR, Medina JL, Dube PH, Shapiro MS and Brenner R (2013) Functional effects of KCNQ K+ channels in airway smooth muscle. Front. Physiol. 4:277. doi: 10.3389/fphys.2013.00277
- Medina, J.L., Coalson, J.J., Brooks, E.G., Winter, V.T., Chaparro, A., Principe, M.,Kannan, T.R., Baseman, J.B., and Peter H. Dube. 2012. Mycoplasma pneumoniae CARDS toxin induces pulmonary eosinophilic and lymphocytic inflammation. Am J Respir Cell Mol Biol Jun;46(6):815-22 PMID: 22281984
- Bose, R., Thinwa, J., Chaparro, A., Zhong, Y., Zhong., G, Bose, S., and Dube, P.H., 2011. MAPkinase-dependent IL-1alpha intracrine signaling is modulated by YopP during Y. enterocolitica infection. Infect and Immun. Jan;80(1):289-97 PMID: 22083707
- Embry, A. E., Meng, X, Cantwell, A.M., Dube, P.H.,* and Yan Xiang.,* 2011. Enhancement of Immune Response to an Antigen Delivered by Vaccinia Virus by Displaying the Antigen on the Surface of Intracellular Mature Virion. Vaccine Jul 26;29(33):5331-9* corresponding authors PMID: 21664218
- Cantwell, A. M., Bubeck, S., and Dube, P.H., 2010. YopH inhibits early pro-inflammatory cytokine responses during plague pneumonia. BMC Immunology. 11:29 PMID: 20565713
- Zhong, Y., Cantwell, A.M., and Dube, P.H. 2010. Transforming growth factor-beta and CD-25 is important for controlling systemic dissemination following Yersinia enterocolitica infection. Infect and Immun. 78:3716-3725 PMID: 20584975
- Hardy, R.D., Coalson,J.J., Peters, J.,Chapparo, A., Cantwell, A.M., Kannan, T.R., Baseman, J.B., and Dube, P.H. 2009. Analysis of pulmonary inflammation and function in the mouse and baboon after exposure to Mycoplasma pneumoniae CARDS toxin. Plos one. 4:e7562. PMID: 19859545
- Dube, P. 2009 Interaction of Yersinia with the gut: mechanisms of pathogenesis and immune evasion.
- Curr. Top. Microbiol. Immunol. 337:61-91 PMID: 19812980
- Sabbah, A., Chang, T.H., Harnack, R., Frolich, V.C., Tominaga, K., Dube, P.H., Berton, M.T., Xiang, Y., and Bose, S. 2009. Activation of innate immune antiviral response by NOD2. Nat. Immunol. 10:1073- 1080. PMID: 19701189
- Xiaoyun Zhang, Gao, L., Lei L., Zhong, Y., Dube, P., Berton, M., Arulanandam, B., Zhang, J., and Zhong, G. 2009. A MyD88-dependent early IL-17 production protects mice against airway infection with the obligate intracellular pathogen Chlamydia muridarum. J. Immunol. 183:1291-1300 PMID: 19542374