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bacterial pathogenesis, Escherichia coli, host-pathogen interactions, innate immunity, nanotechnology, urinary tract infection

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6th Floor, McDonnell Pediatric Research Bldg



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The lab studies the interactions of pathogenic Gram-negative bacteria with host epithelial surfaces and immune effectors. In particular, we are investigating the modulation of host immune responses by pathogens and the mechanisms by which these bacteria present specific virulence factors on their surfaces. We utilize a robust bacterial genetic system coupled with cultured bladder cell models and the mouse model of cystitis, which has recently been employed to advance new paradigms regarding the pathogenesis of urinary tract infections (UTI). The most common cause of UTI, uropathogenic Escherichia coli (UPEC), has been shown to invade bladder epithelial cells, replicate within these cells to form intracellular bacterial communities, and persist within a quiescent bacterial reservoir that is undetected by host immune mechanisms. Current projects in our lab include (1) delineating the genetic basis for the ability of UPEC to downregulate host cell inflammatory signaling, facilitating bacterial persistence within the bladder; (2) studying host and bacterial transcriptional programs active during the interaction of UPEC with human neutrophils; (3) characterizing outer membrane protein virulence factors in UPEC during UTI; and (4) engineering antimicrobial nanoparticles coated with bacterial adhesins for use in prevention of acute and recurrent UTI. Our goals are to discover novel targets for interventions that will prevent and treat Gram-negative epithelial infections. We also participate in translational studies of pediatric infections caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA).

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David A. Hunstad

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Exploration of novel virulence mechanisms and therapeutics in E. coli urinary tract infection

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Date Last Updated

11/10/2011 10:36 AM


Loughman JA, Hunstad DA.  Attenuation of human neutrophil migration and function by uropathogenic bacteria. Microbes Infect 2011 13: 555-565. PMCID: PMC3092803
Horvath DJ, Li B, Casper T, Partida-Sanchez S, Hunstad DA, Hultgren SJ, Justice SS.  Morphological plasticity promotes resistance to phagocyte killing of uropathogenic Escherichia coli. Microbes Infect 2011 13: 426-437. PMCID: PMC3071881
Hunstad DA, Justice SS.  Intracellular lifestyles and immune evasion strategies of uropathogenic Escherichia coli. Annu Rev Microbiol 2010 64: 203-221.
Li Y, Hindi K, Watts KM, Taylor JB, Zhang K, Li Z, Hunstad DA, Cannon CL, Youngs WJ, Wooley KL (2010). Shell crosslinked nanoparticles carrying silver antimicrobials as therapeutics. Chem Commun 46: 121-123. PMCID: PMC2978063
Nicholson TF, Watts KM, Hunstad DA.  OmpA of uropathogenic Escherichia coli promotes post-invasion pathogenesis of cystitis. Infect Immun 2009 77: 5245-5251. PMCID: PMC2786482
Loughman JA, Fritz SA, Storch GA, Hunstad DA.  Virulence gene expression in human community-acquired Staphylococcus aureus infection. J Infect Dis 2009 199: 294-301. PMCID: PMC2843142
Orscheln RC*, Hunstad DA*, Fritz SA, Loughman JA, Mitchell K, Storch EK, Gaudreault M, Sellenriek PL, Armstrong JR, Mardis ER, Storch GA.  Contribution of genetically restricted, methicillin-susceptible strains to the ongoing epidemic of community-acquired Staphylococcus aureus infections. Clin Infect Dis 2009 49: 536-542. PMCID: PMC2965061
Watts KM, Hunstad DA.  Components of SurA required for outer membrane biogenesis in uropathogenic Escherichia coli. PLoS One 2008 3: e3359.
Justice SS, Hunstad DA, Seed PC, Hultgren SJ.  Filamentation by Escherichia coli subverts innate defenses during urinary tract infection. Proc Natl Acad Sci USA 2006 2006103: 19884-19889.

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Created at 11/10/2011 10:36 AM by DBBS_SP_SAPP
Last modified at 11/10/2011 11:40 AM by Kathryn Ruzicka