PHARMACOLOGY ::   P. DAVID ROGERS, PHARM.D., PH.D., FCCP      drogers@utmem.edu  
 
 Publications :: Associate Professor of Clinical Pharmacy, Pharmaceutical Sciences, Pediatrics and Molecular Sciences

The fungus Candida albicans is a cause of mucosal, cutaneous, and systemic infections, including oropharyngeal candidiasis (OPC), the most frequent opportunistic infection among AIDS patients. Furthermore, bloodstream infections due to Candida species are an increasingly important complication in hospitalized patients. In the United States, candidemia is the fourth most common nosocomial bloodstream infection, has a significant impact on mortality rates, and is associated with excessive morbidity and prolongation of hospital stay. The interests of Dr. David Rogers’ lab revolve around three areas central to the management of infections due to C. albicans: 1) the molecular basis for the mechanism of specific antifungal agents; 2) molecular mechanisms of antifungal resistance; and 3) the role of the innate immune response in the interaction between C. albicans and the host. With the recent sequencing of the C. albicans genome, his group has made use of new technologies that have subsequently become available to the field of Candida research. These studies have clarified the molecular basis of azole resistance and have identified new molecules for further study. It is their hope that newly identified mediators of this phenotype will serve as targets for the development of therapeutic strategies to circumvent resistance and improve the therapeutic index of the azole antifungal agents.

Rogers PD, Lewis RE, Kramer RE. Extracellular calcium is not associated with the activity of amphotericin B against Candida albicans. J Antimicrob Chemother 2003; 51:305-312

Rogers PD, Barker KS, Herring V. Heat-induced superaggregation of amphotericin B attenuates its ability to induce cytokine and chemokine production in the human mono-cytic cell line THP-1. J Antimicrob Chemother 2003; 51:405-408

Barker KS, Liu T, Rogers PD. Analysis of differential gene expression in the human monocytic cell line THP-1 in response to Candida albicans. J Infectious Dis 2005; 192:901-912

Liu, TT, Lee REB, Barker KS, Lee RE, Wei L, Homayouni R, Rogers PD. Genome-wide expression profiling of the response to azole, polyene, echinocandin, and pyrimidine antifungal agents in Candida albicans. Antimicrob Agents Chemother 2005; 49:2226-2236

Lee REB, Liu TT, Barker KS, Lee RE, Rogers PD. Genome-wide expression profiling of the response to ciclopirox olamine in Candida albicans. J Antimicrob Chemother 2005; 55:655-662

Vermitsky JP, Earhart KE, Smith L, Homayouni R, Edlind TE, Rogers PD. PDR1 regulates multidrug resistance in Candida glabrata: gene disruption and genome-wide expression studies. Mol Microbiol 2006, 61:704-722

Rogers PD, Vermitski JP, Edlind TD, Hilliard GM. Proteomic analysis of experimentally induced azole resistance in Candida glabrata. J Antimicrob Chemother 2006, 58: 434-438

 

 
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