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Departments

Education

  • Ph.D., University of Texas Health Science Center at San Antonio, 2014
  • M.S., Texas A&M International University, 2008
  • B.S., Baylor University, 2004

Courses

  • Genetic Principles
  • Cell and Molecular Methods
  • Biology - Lecture and Lab

Biography

Jesus A. Segovia, Ph.D., received his bachelor’s degree in Biology from Baylor University in 2004. He then attended graduate school at Texas A&M International University and earned a master’s degree in Biology, with a focus in Microbiology, in 2008. In 2009, he joined the Department of Microbiology and Immunology at the University of Texas Health Science Center at San Antonio. In early 2010, Segovia joined the laboratory of Santanu Bose to pursue his Ph.D. in the field of innate immunity and inflammation.

Segovia’s research was aimed at characterizing the mechanism by which respiratory syncytial virus (RSV) activates the inflammasome complex. The inflammasome complex is a multi-protein complex that mediates activation of caspase-1, an inflammatory enzyme that catalyzes the activation of the inflammatory cytokines IL-1β and IL-18. The activation of this complex is critical for initiating the inflammatory response and orchestrating the adaptive immune response during infection.

After earning his Ph.D., Segovia joined the Baseman laboratory in 2014 to pursue research focused on characterizing the molecular mechanisms that activate and regulate the innate immune response to Mycoplasma pneumoniae infection. His studies have uncovered a critical role for the NLRP3 inflammasome complex in initiating the acute inflammatory response during M. pneumoniae infection. His findings have profound implications due to his part in the recent discovery that NLRP3 is post-translationally modified (and activated) by the unique ADP-ribosylating and vacuolating CARDS toxin produced by M. pneumoniae.  Currently, he is initiating numerous undergraduate research projects focused on characterizing the mechanisms of inflammation during M. pneumoniae infection, including how the ADP-ribosylation activity of CARDS Toxin affects mitochondrial function and how the vacuolization activity of CARDS toxin affects monocytes and epithelial cells.

Publications

Shil N, Mainali Pokharel S, Segovia JA, Tsai S-Y, Chang T-H and Bose S. 25-hydroxycholesterol activates integrin-FAK signaling and links TLR, Nod2, TNFR pathways with signaling to intensify inflammatory response. Commun. (in press)

Segovia JA, Chang TH, Winter VT, Coalson JJ, Cagle MP, Pandranki, L Bose S, Baseman JB and Kannan TR. NLRP3 is a critical regulator of inflammation and innate immune cell response during Mycoplasma pneumoniae Infect Immun (2017). PMCID: PMC5736809

Lizcano A, Akula Suresh Babu R, Shenoy AT, Saville AM, Kumar N, D’Mello A, Hinojosa CA, Gilley RP, Segovia JA, Mitchell TJ, Tettelin H and Orihuela CJ. Transcriptional organization of pneumococcal psrP-secY2A2 and impact of GtfA and GtfB deletion on PsrP-associated virulence properties. Microbes Infect (2017)

Tsai SY, Segovia JA, Chang TH, Shil NK, Pokharel SM, Kannan TR, Baseman JB, Pagé N, Cesaro A, Tessier PA and Bose S. Regulation of TLR3 activation by S100A9. J Immunol doi:10.4049/jimmunol.1500378 (2015). PMCID: PMC4747058

Segovia JA, Chang TH, Tsai SY, Hakala KW, Weintraub ST, Short JD and Bose S. Nedd8 regulates inflammasome-dependent caspase-1 activation. Mol Cell Biol 35(3):582—597 (2015). PMCID: PMC4285429

Bose S, Segovia JA, Somarajan SR, Chang TH, Kannan TR and Baseman JB. ADP-ribosylation of NLRP3 by Mycoplasma pneumoniae CARDS toxin regulates inflammasome activity. MBio 5(6):e02186-14 (2015). PMCID: PMC4278538

Thinwa J, Segovia JA, Bose S and Dube PH. Integrin-mediated pathogen recognition leads to inflammasome-dependent IL-18 secretion from intestinal epithelial cells. J Immunol 193(3):1373-82 (2014). PMCID: PMC4174679

Tsai SY, Segovia JA, Mgbemena V, Chang TH, Morris IR, Berton MT, Tessier PA, Tardif MR, Cesaro A and Bose S. DAMP molecule S100A9 acts as a molecule pattern to enhance inflammation during Influenza A Virus infection: Role of DDX21-TRIF-TLR4-MyD88 pathway. PLoS Pathog 10(1): e1003848 (2014) doi:10.1371/journal.ppat.1003848. PMCID: PMC3879357

 

Mgbemena V*, Segovia JA*, Chang TH and Bose S. KLF6 and iNOS regulates apoptosis during respiratory syncytial virus infection. Cell Immunol 283(1-2):1-7 (2013). PMCID: PMC3744625 *Co-first authors

Mgbemena V*, Segovia JA*, Chang TH, Tsai SY, Cole GT, Hung CY and Bose S. Transactivation of inducible nitric oxide synthase gene by Krüppel-like factor 6 regulates apoptosis during influenza A virus infection. J Immunol 189(2):606—615 (2012). PMCID: PMC3392426 *Co-first authors

Segovia JA, Sabbah A, Mgbemena V, Tsai SY, Chang TH, Berton M, Morris IR, Allen IC, Ting JP and Bose S. TLR2/MyD88/NF-κB pathway, reactive oxygen species, potassium efflux activates NLRP3/ASC inflammasome during respiratory syncytial virus infection. PLoS One 7:e29695 (2012). PMCID: PMC3266238

Chang TH, Segovia JA, Sabbah A, Mgbemena V and Bose S. Cholesterol-rich lipid rafts are required for release of infectious human respiratory syncytial virus particles. Virology 422: 205—211 (2012). PMCID: PMC3249476

Mgbemena V, Segovia JA, Chang TH and Bose S. Krüppel-like factor 6 regulates transforming growth factor-β gene expression during human respiratory syncytial virus infection. Virology J 8:409—415 (2011). PMCID: PMC3170303

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