Wilmara Salgado Pabón


Department of Pathobiological Sciences
Office: 4370

Wilmara Salgado Pabón

Titles and Education

  1. 2000 – B.S. Medical Microbiology and Immunology, UW-Madison
  2. 2002 – M.S. Medical Microbiology and Immunology, Dr. Gerald I. Byrne, UW-Madison

  3. 2008 – PhD Microbiology, Dr. Joseph P. Dillard, UW-Madison

  4. 2011 – Postdoctoral Fellow, Cell Biology and Infection, Dr. Philippe J. Sansonetti, Institut Pasteur, Paris

  5. 2013 – Postdoctoral Fellow, Microbiology and Immunology, Drs. Patrick M. Schlievert and Alexander R. Horswill, UIowa


My research program focuses on the pathogenesis of Staphylococcus aureus with an emphasis on the contribution of enterotoxins and cytolysins to the pathophysiology of severe disease, including (but not limited to) sepsis, pneumonia, and infective endocarditis. The long-term goal of my research program is to dissect the S. aureus mechanisms leading to these life-threatening illnesses at the molecular, cellular and whole system level. The laboratory is currently funded by an R01 grant from NIAID to study infective endocarditis. We are taking students and post-docs. Come join us!

Infective endocarditis (IE) research focus:
S. aureus enterotoxins are major virulence factors in human and animal isolates. Superantigenicity (a hallmark feature of S. aureus enterotoxins) results in a T cell dependent cytokine storm leading to inflammatory syndromes. Non-hematopoietic cell interactions of enterotoxins are not well-known and poorly characterized, yet our evidence suggest that it significantly contributes to pathogenesis. A central question is then, how do these biological properties drive IE development and progression?  We are currently addressing this central question utilizing isogenic infective endocarditis deficient strains complemented to produce toxoids deficient in specific functions. Studies in rabbit models of pneumonia will follow. We are also characterizing the non-hematopoietic interaction of enterotoxins in in vitro systems to be followed by testing in disease models.

Endothelial cells lining the vasculature are exposed to a great variety of bloodborne stimuli and are in fact one of the first cell types to detect and respond to these stimuli, including circulating pathogens and their toxins. Pathological changes to the endothelium can result in dysregulated innate immune system activation and defects in wound healing. We are performing RNAseq analysis of endothelial cells treated with enterotoxins or cytolysins to gain a broader sense of the pathways activated or manipulated by these toxins. We will also use the rabbit aortic explant culture model and rabbit models of toxemia and bacteremia to elucidate mechanisms ex vivo and in vivo. At the end, we would have defined endothelial cell functions targeted by specific S. aureus toxins and potential mechanisms contributing to tissue injury. In turn, we will be able to address whether disease outcomes can be improved by intervention strategies targeting the endothelium.

Recent Publications

  1. ϕSa3mw Prophage as a Molecular Regulatory Switch of Staphylococcus aureus β-Toxin Production.

    Tran PM, Feiss M, Kinney KJ, Salgado-Pabón W.

    J Bacteriol. 2019 Jun 21;201(14). pii: e00766-18. doi: 10.1128/JB.00766-18. Print 2019 Jul 15.

  2. The Superantigen Toxic Shock Syndrome Toxin 1 Alters Human Aortic Endothelial Cell Function.

    Kulhankova K, Kinney KJ, Stach JM, Gourronc FA, Grumbach IM, Klingelhutz AJ, Salgado-Pabón W.

    Infect Immun. 2018 Feb 20;86(3). pii: e00848-17. doi: 10.1128/IAI.00848-17. Print 2018 Mar.

  3. Staphylococcal β-Toxin Modulates Human Aortic Endothelial Cell and Platelet Function through Sphingomyelinase and Biofilm Ligase Activities.

    Herrera A, Kulhankova K, Sonkar VK, Dayal S, Klingelhutz AJ, Salgado-Pabón W, Schlievert PM.

    MBio. 2017 Mar 21;8(2). pii: e00273-17. doi: 10.1128/mBio.00273-17.

  4. The Spl Serine Proteases Modulate Staphylococcus aureus Protein Production and Virulence in a Rabbit Model of Pneumonia.

    Paharik AE, Salgado-Pabon W, Meyerholz DK, White MJ, Schlievert PM, Horswill AR.

    mSphere. 2016 Oct 12;1(5). pii: e00208-16. eCollection 2016 Sep-Oct.

  5. Phenotypes and Virulence among Staphylococcus aureus USA100, USA200, USA300, USA400, and USA600 Clonal Lineages.

    King JM, Kulhankova K, Stach CS, Vu BG, Salgado-Pabón W.

    mSphere. 2016 Jun 8;1(3). pii: e00071-16. doi: 10.1128/mSphere.00071-16. eCollection 2016 May-Jun.

  6. The Staphylococcus aureus Global Regulator MgrA Modulates Clumping and Virulence by Controlling Surface Protein Expression.

    Crosby HA, Schlievert PM, Merriman JA, King JM, Salgado-Pabón W, Horswill AR.

    PLoS Pathog. 2016 May 4;12(5):e1005604. doi: 10.1371/journal.ppat.1005604. eCollection 2016 May.

  7. Novel Tissue Level Effects of the Staphylococcus aureus Enterotoxin Gene Cluster Are Essential for Infective Endocarditis.

    Stach CS, Vu BG, Merriman JA, Herrera A, Cahill MP, Schlievert PM, Salgado-Pabón W.

    PLoS One. 2016 Apr 28;11(4):e0154762. doi: 10.1371/journal.pone.0154762. eCollection 2016.

  8. Staphylococcus aureus β-Toxin Mutants Are Defective in Biofilm Ligase and Sphingomyelinase Activity, and Causation of Infective Endocarditis and Sepsis.

    Herrera A, Vu BG, Stach CS, Merriman JA, Horswill AR, Salgado-Pabón W, Schlievert PM.

    Biochemistry. 2016 May 3;55(17):2510-7. doi: 10.1021/acs.biochem.6b00083. Epub 2016 Apr 15.

  9. Aortic Valve Damage for the Study of Left-Sided, Native Valve Infective Endocarditis in Rabbits.

    Salgado-Pabón W, Schlievert PM.

    Methods Mol Biol. 2016;1396:73-80. doi: 10.1007/978-1-4939-3344-0_6.

  10. Does Staphylococcus aureus have a role in the development of Type 2 diabetes mellitus?

    Schlievert PM, Salgado-Pabón W, Klingelhutz AJ.

    Future Microbiol. 2015;10(10):1549-52. doi: 10.2217/fmb.15.95. Epub 2015 Oct 6. No abstract available.

  11. Full list of publications can be found here: https://www.ncbi.nlm.nih.gov/pubmed/?term=salgado-pabon.