Francis Alonzo, Ph.D.
Ph.D., University of Illinois at Chicago
Major Research Interests: We are interested in investigating the molecular mechanisms underlying Staphylococcus aureus disease processes and bacterial evasion of the host immune response.
For a bacterial pathogen to cause disease it often must: acquire metabolic resources from nutrient restricted environments; escape host immune defenses; produce virulence factors that damage host cells or usurp host functions; and/or use physical means to persist in inhospitable conditions. My laboratory aims to develop a better understanding of these pathogenic mechanisms in the bacterium Staphylococcus aureus. Specifically, we are interested in determining how S. aureus adjusts from a lifestyle as a transient commensal to a virulent pathogen through metabolic adaptation and evasion of host immune defenses. S. aureus is a leading cause of nosocomial infection in the United States and is a predominant pathogen in communities. Infections caused by S. aureus result in diseases that include skin lesions, pneumonia, osteomyelitis, endocarditis, and bacteremia. Complicating treatment of S. aureus infection is the recent rise in multidrug resistant infectious isolates. The overwhelming number of resistant clones highlights a need for novel treatment modalities that refrain from reliance on antibiotic usage. The ability of S. aureus to infect a host is influenced by its subversion of host immunity. We are currently investigating the mechanisms of action of a number of novel immunomodulatory factors produced by S. aureus that appear to perturb macrophage pro-inflammatory activity. This modulation of macrophage function enhances pathogenic outcomes during infection. Our research uses elements of bacterial genetics, biochemistry, immunology, cell biology, as well as murine infection models to define how these factors modulate macrophage function in vitro and in vivo, ultimately allowing us to determine how S. aureus subverts immune defenses. In addition, we use similar experimental techniques to investigate the effects of nutritional restriction within host tissues on S. aureus viability. In doing so, we aim to identify novel mechanisms by which S. aureus metabolically adapts to life inside an infected host. Ultimately, these studies have the potential to increase our understanding of S. aureus adaptation during infection. We anticipate this work will stimulate the development of novel therapeutics designed to treat diseases cause by S. aureus with potential applicability to pathogens that behave similarly.
Alonzo F. 3rd, Benson MA, Chen J, Novick RP, Shopsin B, Torres VJ. (2012) Staphylococcus aureus leukocidin ED contributes to systemic infection by targeting neutrophils and promoting bacterial growth in vivo. Mol. Microbiol. 83(2):423-35. PMID: 22142035
Alonzo F. 3rd, Kozhaya L, Rawlings SA, Reyes-Robles T, DuMont AL, Myszka DG, Landau NR, Unutmaz D, Torres VJ. (2013) CCR5 is a receptor for Staphylococcus aureus Leukotoxin ED. Nature. 493(7430):51-5. PMID: 23235831
Alonzo F. 3rd, Torres VJ. (2013) Bacterial survival amidst an immune onslaught: the contribution of the Staphylococcus aureus leukotoxins. Pearls Review Article, PLoS Pathogens. 9(2): e1003143. PMID:23436994.
Reyes-Robles T*, Alonzo F 3rd*, Kozhaya L, Lacey DB, Unutmaz D, Torres VJ. (2013). Staphylococcus aureus targets CXCR1/CXCR2 to kill leukocytes and promote infection. Cell Host and Microbe. 14(4):453-9. *Contributed Equally.
Alonzo F 3rd and Torres VJ (2014). Staphylococcus aureus bi-component leucocidins. Microbiology and Molecular Biology Reviews. 78(2):199-230. PMID: 24847020
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