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Andrés Vázquez-Torres, D.V.M., Ph.D.

Professor of Immunology & Microbiology

12800 E. 19th Ave., RC-1 N 9131
Mail Stop 8333, Aurora, CO 80045
Phone: (303) 724-4218

Dr. Vázquez-Torres received his DVM from the University of Córdoba, Spain, and his Ph.D. from the University of Wisconsin-Madison. He is a Professor of Immunology and Microbiology at the University of Colorado School of Medicine, and is Director of a T32 pre-doctoral training program. He has served on multiple study sections and editorial boards, and has been honored for Teaching Excellence. He has received awards from the Spanish Ministry of Education, NRSA, Schweppe Foundation, Burroughs Wellcome Fund, and ASM Merck Irving S. Sigal Memorial. His laboratory studies redox active thiol-based sensors in bacterial resistance to the antimicrobial actions of host NADPH phagocyte oxidase and inducible nitric oxide synthase hemoproteins. This research is uncovering novel bacterial mechanisms of redox sensing, antioxidant and antinitrosative defense, antibiotic tolerance, metabolic adaptation, and virulence. VA, and F, K, R and T NIH grants to him or his trainees fund the Vazquez-Torres' lab.

Dr. Vazquez-Torres is a Professor of Immunology and Microbiology at the University of Colorado School of Medicine. Using the bacterial pathogen Salmonella as model microorganism, he studies sensing of and adaptation to oxidative and nitrosative stress.

Infectious diarrhea is a complex syndrome caused by many viruses, parasites, fungi and bacteria such as Salmonella. Salmonellosis itself encompasses a spectrum of clinical diseases that range from enteric fever, a serious condition that kills about 600,000 people a year, to non-typhoidal zoonotic infections that affect over a billion people worldwide and more than a million Americans annually. Treatment of Salmonella and medically important Gram-negative rods is often complicated by the increasing resistance of pathogenic bacteria to antibiotics used in the clinic. In the course of human infection, Salmonella are exposed to reactive oxygen and nitrogen species produced by the NADPH phagocyte oxidase and inducible nitric oxide synthase (iNOS). Clinical and experimental observations indicate that these reactive species mediate host defense against Salmonella. However, Salmonella and a variety of clinically relevant Gram-positive and –negative bacteria can co-opt reactive oxygen and nitrogen species to foster virulence and gain resistance to various classes of antibiotics. The research in the Vázquez-Torres lab uses state-of-the-art biochemical, genetic and molecular biology approaches to understand the molecular mechanisms by which reactive species mediate resistance of macrophages against intracellular bacteria, as well as the adaptive strategies that boost antioxidant and antinitrosative defenses of pathogenic bacteria.

The survival of Salmonella within macrophages is greatly dependent on the type III secretion system encoded within the Salmonella pathogenecity island 2 (SPI2). Our investigations have found that the type III secretion system encoded in the Salmonella pathogenecity island 2 (SPI2) blocks the interactions of Salmonella vacuoles with NADPH oxidase-containing vesicles and lysosomes, thereby inhibiting the progression of the Salmonella phagosome along the degradative pathway. However, the high throughput of nitric oxide generated by macrophages in response to IFNγ inhibits the transcription of the SPI2 type III secretion system, thus allowing maturation of the Salmonella phagosome for fusion with lysosomes. The expression of SPI2 is controlled by the SsrA/SsrB two-component regulatory system. In addition to canonical phosphorylation, our investigations indicate that SsrB is also under the post-translational control of oxidation and S-nitrosylation, and that the sensing of reactive species through Cys203 in the dimerization domain of SsrB fosters Salmonella pathogenesis. Moreover, our research indicates that SsrB is also regulated via protein-protein interactions with a chaperon already present in ancestral lineages of enterobacteriaceae.

First associated with nutritional deprivation, the “stringent response” activates or represses global gene transcription through the actions of the guanine tetraphosphate (ppGpp) alarmone and the DksA regulatory protein on the RNA polymerase (RNAP).  The stringent response protects phylogenetically diverse eubacteria against a variety of environmental stress conditions and promotes the virulence of medically important pathogens such as Pseudomonas aeruginosa, Vibrio cholerae, and Salmonella enterica. Our recent work indicates that reactive oxygen and nitrogen species elicit a stringent response in Salmonella.  Our investigations have identified the zinc finger in the globular domain of DksA as a bone fide sensor of oxidative and nitrosative stress. We are actively testing the hypothesis that the sensing of reactive species by the DksA zinc finger promotes antioxidant and antinitrosative defenses, antibiotic resistance and the pathogenicity of Salmonella. Given that most Gram-negative bacteria express DksA orthologues with a conserved zinc finger, our investigations are likely generalizable to a variety of clinically important, and phylogenetically diverse pathogenic bacteria.

The investigations in the Vázquez-Torres lab are funded by grants from the National Institute of Health, the Veterans Administration, and the Burroughs Wellcome Fund.

Dr. Vázquez-Torres was the recipient of a fellowship from the Spanish Ministry of Sciences and Education in 1983 and an Individual National Research Service Award from the Department of Health and Human Services, 1998-2001. Since joining the faculty at the University of Colorado at Denver School of Medicine in 2001, he has received five Excellence in Teaching Awards and has won a prestigious Schweppe Foundation Career Development Award. In 2004, he was presented with the Merck Irving S. Sigal Memorial Award at the 104th General Meeting of the American Society for Microbiology. He is also a 2007 recipient of the Burroughs Wellcome Fund Investigators in Pathogenesis of Infectious Diseases Award. Dr. Vázquez-Torres was a regular Member of the Bacterial Pathogenesis Study Section, National Institutes of Health, and is a frequent ad hoc reviewer in numerous national and international study sections. He is a member of the Microbiology and Molecular Biology Graduate Programs. In 2010, he became the Director of the Molecular Pathogenesis of Infectious Diseases pre-doctoral T32 training program. He is in the editorial board of Infection and Immunity, and Frontiers in Cellular Microbiology; he is also an editor for Scientific Reports.

OMB No. 0925-0046, Biographical Sketch Format Page

OMB No. 0925-0001 and 0925-0002 (Rev. 10/15 Approved Through 10/31/2018)


Provide the following information for the Senior/key personnel and other significant contributors.
Follow this format for each person.  DO NOT EXCEED FIVE PAGES.

NAME: Andres Vazquez-Torres, D.V.M., Ph.D.

eRA COMMONS USER NAME (credential, e.g., agency login): Vazquez-Torres


EDUCATION/TRAINING (Begin with baccalaureate or other initial professional education, such as nursing, include postdoctoral training and residency training if applicable. Add/delete rows as necessary.)



(if applicable)


Completion Date





University of Córdoba, Córdoba, Spain



Vet. Medicine

University of Wisconsin, Madison, WI



Microbial Pathogenesis

University of Wisconsin, Madison, WI



Microbial Pathogenesis


A. Personal Statement. The Vázquez-Torres’ lab studies the molecular mechanisms by which redox active sensors of reactive oxygen and nitrogen species regulate transcription of genes essential for bacterial pathogenesis as well as the function of antioxidant and antinitrosative defenses that protect intracellular pathogens against the actions of the NADPH phagocyte oxidase and inducible nitric oxide synthase hemoproteins. The long-term goal of the Vazquez-Torres’ lab is to understand how sensing of oxidative and nitrosative stress by redox-active bacterial regulatory proteins promotes antioxidant and antinitrosative defenses, antibiotic resistance, and pathogenicity. These investigations are conducted in the clinically important pathogens Salmonella, and Burkholderia. The basic mechanisms uncovered in these microorganisms are likely generalizable to a variety of clinically important, phylogenetically diverse pathogenic bacteria. The fundamental processes studied in our lab are leading to the identification of new antibiotics against evolutionarily conserved bacterial targets.


B. Positions, Honors, and Awards.


1987-1989: Intern, Department of Parasitology, Veterinary School, University of Córdoba, Spain.

1989-1990: Visiting Scientist, National Wildlife Health Research Center, Madison, WI.

1990-1991: Visiting Scientist, Department of Animal Health and Biomedical Sciences, and Department of Poultry Sciences, University of Wisconsin-Madison.

1991-1996: Graduate Student, Laboratory of Edward Balish, Ph.D.; Department of Animal Health and Biomedical Sciences; University of Wisconsin-Madison.

1996-2001: Post-Doctoral Fellow, Laboratory of Ferric C. Fang, M.D.; Division of Infectious Diseases; University of Colorado Health Sciences Center.

2001-2008: Assistant Professor, Department of Microbiology; University of Colorado Health Sciences Center.

2005-present: Biomedical Sciences Program Faculty, University of Colorado School of Medicine.

2005-present: Medical Scientist Training Program Faculty, University of Colorado School of Medicine.

2008-2013: Associate Professor with Tenure; Department of Microbiology; University of Colorado School of Medicine.

2010-present: Program Director of the multi-departmental T32 pre-doctoral training grant to study Molecular Pathogenesis of Infectious Diseases.

2012-present: Department of Veterans Affairs and the Department of Defense Medical Research Service Non-Clinician Scientist Intramural Career Program.

2012-present: University of Colorado School of Medicine Molecular Biology Graduate Program.

2013-present: Professor with Tenure, Department of Immunology and Microbiology, University of Colorado School of Medicine.



Memberships in NIH Study Sections. NIH Bacterial Pathogenesis Study Section (2007-11); NIH T32 Microbiology and Infectious Diseases (MID) (2015-2019).

Ad hoc Member Study Sections. NIH Bacteriology and Mycology ZRG1 BM-1  (2003); NIH Innate Immunity and Inflammation (III) (2005); NIH Host Interactions with Bacterial Pathogens (2007); Argentinean National Agency for the Promotion of Science and Technology (2001-2005); Wellcome Trust (2001-2004); the European Science Foundation (2009); INFB Merit VA Study Section (2011-2015); NIH T32 Microbiology and Infectious Diseases MID-B (2014); NIH Topics in Bacterial Pathogenesis IDM-B (2015).

Editorial Board Member for the journals Infection and Immunity (since 2010) and Frontiers in Cellular Microbiology (since 2010).

Associate Editor for Scientific Reports (since 2011).

Ad hoc Reviewer for the Journals: Antioxidants & Redox Signaling; Am J Physiol; Cell Host Microbe; Cell Microbiol; FEMS Microbiol Letters; Free Radical Biol Med; Immunology; J Clin Microbiol; J Exp Med; J Infect Dis; J Leuk Biol; mBio; Microbes Infect; Microbial Pathogenesis; Microbiology; Mol Microbiol; Nitric Oxide; PLoS ONE; PLoS Pathogens; Traffic; Vaccine; Virulence.

Society Memberships: American Society of Microbiology; American Academy for the Advancement of Science; American Society for Biochemistry and Molecular Biology.

Committee Memberships: Advisory Committee, Boulder 3-D Lab, P01 project (2005); Steering Committee for the Rocky Mountain Research Center of Excellence (2009-2014); Postdoctoral Association Committee, University of Colorado School of Medicine (2008-2009); University of Colorado School of Medicine Faculty Promotions and Tenure Committee (2010-2012); University of Colorado School of Medicine Rules and Governance Committee (2012); External Advisory Committee for the T32 Training Program in Comparative Medicine, College of Veterinary Medicine, Cornell University (2014-present); Vice Chancellor’s Advisory Committee University of Colorado Denver (2014-present).


Spanish Ministry of Science and Education Merit Fellowship (1983-1984).

F32 Individual National Research Service Award, Department of Health and Human Services (1998-2001).

Schweppe Career Development Award from the Schweppe Foundation (2003-2004).  

Merck Irving S. Sigal Memorial 2004 Award by the American Academy of Microbiology (2004).

Burroughs Wellcome Fund Investigators in Pathogenesis of Infectious Diseases Award (2007).

Excellence in Teaching Awards presented by the Sophomore Medical Class of the University of Colorado School of Medicine in the academic years 2001-2, 2003-4, 2004-5, and 2010.

Excellence in Teaching Award presented by University of Colorado Microbiology Graduate students in 2005.

Fellow to the American Academy of Microbiology (2016).


C. contributions to science (Selected from 84 original papers, review articles, book chapters, and letters).


Innate immune responses in the gastrointestinal mucosa. Our investigations have contributed to a greater understanding of mucosal immunology. We identified a critical role for nitric oxide (NO) in resistance to mucosal candidiasis. NO produced in response to γδ T cell-generated IFNγ protects mice against gastric candidiasis. We were the first to discover that lamina propria phagocytic cells sample microbes from the gut lumen. The ability of dendritic cells to migrate to systemic sites provides a route for extraintestinal dissemination of pathogenic microorganisms. We now know that this mechanism of antigen sampling from mucosal surfaces is exploited by phylogenetically diverse pathogens, including viruses and bacteria, to gain access to host tissues.

1.         Jones‑Carson, J., A. Vazquez‑Torres, H.C. van der Heyde, T. Warner, R.D. Wagner, & E. Balish. 1995.  γ δ T cell‑induced nitric oxide production enhances resistance to mucosal candidiasis. Nature Med. 1: 552-557.

2.         Vazquez-Torres, A., J. Jones-Carson, A.J. Bäumler, S. Falkow, R. Valdivia, W. Brown, M. Lee, R. Berggren, W.T. Parks, & F.C. Fang.  1999.  Extraintestinal dissemination of Salmonella via CD18-expressing phagocytes.  Nature 401: 804-808.


Antimicrobial mechanisms of mononuclear phagocytic cells. Since I was a student in graduate school at the University of Wisconsin-Madison, I have investigated the mechanisms underlying the potent antimicrobial activity of mononuclear phagocytic cells. I have published seminal investigations on the precise reactive oxygen and nitrogen species used by macrophages in their antimicrobial toolbox. IFNγ-activated macrophages kill the opportunistic pathogen Candida albicans by producing peroxynitrite, a product arising from the condensation of NO and superoxide (O2.-). IFNγ-activated macrophages also use a combination of reactive oxygen and nitrogen species in their antimicrobial activity against the Gram-negative pathogen Salmonella Typhimurium. However, the anti-Salmonella activity of the NADPH phagocyte oxidase and iNOS is manifested in a sequential manner. An early respiratory burst, which is dominated by the the enzymatic activity of NADPH phagocyte oxidase, kills most intracellular Salmonella, whereas reactive nitrogen species produced by iNOS exert late bacteriostatic activity against this intracellular pathogen. The strong nitrosative chemistry that dominates late phases of the innate response of macrophages against Salmonella stems from reactive nitrogen species generated from acidified nitrite in the phagosomal lumen, and N2O3 arising from the second order reaction of NO with molecular oxygen. 

3.         Vazquez-Torres, A., J. Jones-Carson,  & E. Balish. 1996. Peroxynitrite contributes to the candidacidal activity of nitric oxide-producing macrophages.  Infect. Immun. 64: 3127-3133.

4.         Vazquez-Torres, A., J. Jones-Carson, P. Mastroeni, H. Ischiropoulous, & F.C. Fang. 2000. Antimicrobial actions of the NADPH phagocyte oxidase and inducible nitric oxide synthase in experimental salmonellosis.  I. Effects on microbial killing by activated peritoneal macrophages. J.  Exp. Med. 192: 227-236.

5.         McCollister, B.D., J.T. Myers, J. Jones-Carson, M. Husain, & A. Vazquez-Torres. 2008. N2O3 enhances the nitrosative potential of IFNγ-primed macrophages in response to Salmonella. Immunobiology. 212: 759-69. Epub 2007 Dec 3.


Molecular targets of reactive species generated in the innate response. Despite the wide range of biomolecules damaged by reactive species, very few bacterial molecular targets have been identified. We have shown that cytochrome bd of the electron transport chain is a preferred target of NO. Nitrosylation of terminal cytochromes of the electron transport chain arrests replication, thereby exerting bacteriostasis. NO congeners produced by macrophages also inhibit transcription of the SPI2 type III secretion system. Cys203 in the C-terminal dimerization domain of SsrB and PhoP/PhoQ signaling are the molecular targets by which reactive nitrogen species inhibit SPI2 transcription. To the best of our knowledge, these studies were the first to realize that, in addition to the classical phosphorylation signal, bacterial response regulators can be modulated post-translationally by reactive oxygen and nitrogen species.

6.         McCollister, B.D., T. Bourret, R. Gill, J. Jones-Carson, & A. Vazquez-Torres.  2005. Repression of SPI2 transcription by nitric oxide-producing, IFNγ-activated macrophages promotes maturation of Salmonella phagosomes. J. Exp. Med. 202: 625-35.

7.         Husain, M., J. Jones-Carson, M. Song, B.D. McCollister, T.J. Bourret, & A. Vazquez-Torres. 2010. Redox sensor SsrB Cys203 enhances Salmonella fitness against nitric oxide generated in the host immune response to oral infection. Proc Natl Acad Sci U.S.A. 107:14396-401. Epub 2010 Jul 26. Faculty of 1000, 13 Aug 2010.

8.         Husain, M., T.J. Bourret, B.D. McCollister, J. Laughlin, J. Jones-Carson, & A. Vazquez-Torres. 2008. Respiratory arrest evokes an NADH-dependent adaptive response to oxidative stress. J. Biol. Chem. 283: 7682-9. Epub 2008 Jan 15.

9.         Crawford, M.A., T. Tapscott, L.F. Fitzsimmons, L. Liu, A.M. Reyes, S.J. Libby, M. Trujillo, F.C. Fang, R. Radi, & A. Vázquez-Torres. 2016. Redox-active sensing by bacterial DksA transcription factors is determined by cysteine and zinc content. mBio. 7: e02161-15. doi:10.1128/mBio.02161.15.


Novel bacterial defense mechanisms against reactive oxygen and nitrogen species. Our investigations have demonstrated critical roles for glutathione, periplasmic superoxide dismutase, and flavohemoprotein in the antioxidant and antinitrosative arsenal of Salmonella. In addition to these traditional protective mechanisms, Salmonella use a unique defense mechanism to avoid the effects of the NADPH phagocyte oxidase. The type III secretion system encoded within the Salmonella pathogenicity island-2 helps this facultative intracellular pathogen avoid contact with vesicles containing the NADPH phagocyte oxidase. Our recent investigations have demonstrated that expression of the SPI2 type III secretion system is under post-translational control by thioredoxin, a conserved antioxidant system preserved in all branches of life. To our surprise, the canonical thiol-disulfide oxidoreductase activity of thioredoxin is dispensable for regulation of SPI2 expression and antioxidant defense of Salmonella. We have found that the antioxidant defense associated with this ancestral protein is dependent on the interactions of thioredoxin with the flexible linker joining receiver and effector domains of the SPI2 master regulator SsrB. Because thioredoxins are ubiquitous in the bacterial kingdom, the thiol-disulfide oxidoreductase-independent function discovered in our investigations is likely to be a common post-translational mechanism governing protein function. Our investigations have also shown that the global regulatory metalloproteins Fur and FNR coordinate antioxidant and antinitrosative defenses of Salmonella. We have also observed that the RNA polymerase regulatory protein DksA, which is known to regulate the stringent response to nutritional starvation, plays an unexpected and critical role as a sensor of oxidative and nitrosative stress. In addition to playing structural roles critical for the global metabolic adaptation to nutritional stress, we have discovered that thiol groups of cysteine residues in DksA zinc finger help orchestrate transcriptional responses to oxidative and nitrosative stress. Sensing of reactive oxygen and nitrogen species by DksA is essential for Salmonella virulence.

10.       Vazquez-Torres, A., Y. Xu, J. Jones-Carson, D.W. Holden, S.M. Lucia, M. Dinauer, P. Mastroeni, & F.C. Fang. 2000. Salmonella pathogenicity island 2-dependent evasion of the phagocyte NADPH oxidase.  Science. 287: 1655-8.

11.       Henard, C.A., T.J. Bourret, M. Song, & A. Vazquez-Torres. 2010. Control of redox balance by the stringent response regulatory protein promotes antioxidant defenses of Salmonella. J. Biol. Chem. 285: 36785-93. Epub 2010 Sep 17.

12.       Henard, C.A., T. Tapscott, M.A. Crawford, M. Husain, P.T, Doulias, S. Porwollik, L. Liu, M. McClelland, H. Ischiropoulos, & A. Vázquez-Torres. 2014. The 4-Cysteine Zinc-Finger Motif of the RNA Polymerase Regulator DksA serves as a Thiol Switch for Sensing Oxidative and Nitrosative Stress. Mol. Microbiol. Epub 2013 Dec 20. doi: 10.1111/mmi.12498.

13.        Song, M., J.S. Kim, L. Liu, M. Husain, & A. Vazquez-Torres. 2016. Antioxidant defense by thioredoxin can occur independently of canonical thiol-disulfide oxidoreductase enzymatic activity. Cell Reports. 14:1-11.


Host cell inhibition of microbial respiratory activity induces antibiotic tolerance. Despite the strong antimicrobial activity that stems from the nitrosylation of terminal cytochromes of the electron transport chain, diverse bacteria including Salmonella, Burkholderia, and Pseudomonas use the signaling cascade arising from the nitrosylation of terminal cytochromes to reprogram bacterial metabolism, enhance antioxidant defenses, and tolerate antibiotics of clinical relevance. Decreases in oxygen availability also induce antibiotic tolerance. Cumulatively, our investigations indicate that adaptive responses of bacteria to host factors promote resistance of pathogens to antibiotics. 

13.       McCollister, B.D., M. Hoffman, M. Husain, & A. Vazquez-Torres. 2011. Nitric oxide protects bacteria from aminoglycosides by blocking the energy-dependent phases of drug uptake. Antimicrob Agents Chemother. 55: 2189–2196. [Epub 2011 Feb 22].

14.       Jones-Carson, J., A.E. Zweifel, T. Tapscott, C. Austin, J.M. Brown, K.L. Jones, M.I. Voskuil, & A. Vazquez-Torres. 2014. Nitric oxide from IFNγ-primed macrophages modulates the antimicrobial activity of -lactams against the intracellular pathogens Burkholderia pseudomallei and nontyphoidal Salmonella. PLoS Neglected Tropical Diseases. *: e3079.doi:10.1371/journal.pntd.0003079.

15.        Hamad, M.A., C.R. Austin, A.L. Stewart, M. Higgins, A. Vazquez-Torres, & M.I. Voskuil. 2011. Adaptation and antibiotic tolerance of anaerobic Burkholderia pseudomallei. Antimicrob Agents Chemother. 55:3313-23. Epub 2011 May 2.

16.       Vazquez-Torres, A., & A.J. Bäumler. 2016. Nitrate, nitrite and nitric oxide reductases: from the last universal common ancestor to modern bacterial pathogens. Current Opinion Microbiology. 29: 1-8.


For complete list of publications on Pubmed see:


D. Support.

Ongoing funding.


R01 AI5449 NIAID. (PI, A. Vazquez-Torres). Title: “Analysis of intracellular host defenses in Salmonella pathogenesis.”  The major goal of this project is to identify the molecular mechanisms underlying the reactive nitrogen species-mediated repression of Salmonella pathogenicity island-2 transcription. Dr. Vazquez-Torres (PI) is responsible for the overall management of the project and the training of postdoctoral fellows, graduate students, and professional research assistant involved in this project. Dates Approved: 9/30/03 – 05/30/19.


I01BX002073 VA-Merit Award. (PI, A. Vazquez-Torres). Title: “Molecular Analysis of Bacterial Adaptive Response to Host Reactive Species.” The goal is to elucidate the molecular mechanisms by which the RNA polymerase-binding regulatory protein DksA regulates bacterial adaptive responses to oxidative and nitrosative stress. Dates Approved- 04/01/2013-03/30/2017.


Burroughs Wellcome Fund; Investigators in Pathogenesis of Infectious Disease; (PI, A. Vazquez-Torres). Title: “Effects of nitrosative stress on bacterial two component regulatory systems in innate host defense.” The goal is to identify the molecular mechanisms underlying the reactive nitrogen species-mediated inactivation of the PhoPQ two-component regulatory system. Dates Approved- 7/1/2007 – 6/30/2017.


T32 AI052066 Predoctoral Training Grant. (PD, A. Vazquez-Torres). Title: “Molecular Pathogenesis of Infectious Diseases.” The major goals of this pre-doctoral training grant are 1) to educate Ph.D. students in the investigation of fundamental mechanisms by which microbes cause infection, and 2) prepare our graduate students for scientific leadership positions. Dates Approved- 09/30/2003-06/30/2018.


Pending. None.