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Current projects in the lab include:
 
1.  Use of a murine model to study the course of urogenital infection and 
   immune response to C. trachomatis mutant strains (in collaboration with
   Dr. Lutter, OSU).
   Supported by NIH R15 AI119906-01 (2015-2018)
 
 
 
 
Broad Significance: C. trachomatis is the leading cause of infectious blindness; globally there are ~84 million cases of ocular infection.  Approximately three million cases of C. trachomatis sexually transmitted infections are reported each year in the US. Often infection is asympotmatic, may lead to pelvic inflammatory disease, infertility, and increase the risk for cervical cancer. The pathogenesis of chlamydial infection is not fully understood, which has impeded progress toward the development of an effective vaccine. With the recent advances allowing site-directed mutagenesis of chlamydial genes, our labs are testing mutant strains in vivo to better understand the role of specific chlamydial proteins in driving infection and immunity.
 
 
 
2.  Use of a fish model (in collaboration with Dr. Tobler at KSU and 
    Dr. Kelley at WSU) to study mechanisms of tolerance to extreme H2S
    environments.  Our lab's role involves mitochondrial function assays.
    Supported by NSF-IOS (2016-2019)
 
 
 
 
 
Broad Significance: Hydrogen sulfide (H2S), a well known environmental toxin that inhibits cellular respiration, is produced by geothermal and industrial sources. H2S is also a byproduct of cysteine catabolism that, at low levels, drives normal anti-inflammatory, pro-angiogenic and vasodilatory responses in all animals. We are working to understand how extremophile fishes (P. mexicana) are able to maintain aerobic respiration in sulfur springs containing lethal levels of H2S. Our lab is discovering modifications to mitochondrial electron flow that enables these fishes to tolerate toxic H2S. An increased understanding of H2S biology at the cellular level is relevant in ecology, evolutionary biology, and biomedical sciences.
 
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