@article{jayaraman_devlin_miller_scholle_2016, title={The adaptor molecule Trif contributes to murine host defense during Leptospiral infection}, volume={221}, ISSN={["0171-2985"]}, DOI={10.1016/j.imbio.2016.05.006}, abstractNote={Leptospirosis is a zoonotic disease and is caused by pathogenic species of the Leptospira genus, including Leptospira interrogans (L. interrogans). Humans, domestic and wild animals are susceptible to acute or chronic infection. The innate immune response is a critical defense mechanism against Leptospira interrogans, and has been investigated in mouse models. Murine Toll-like receptors (TLRs) have been shown to be key factors in sensing and responding to L. interrogans infection. Specifically, TLR2, TLR4 and the TLR adaptor molecule MyD88 are essential for host defense against L. interrogans; however, the role of the TLR adaptor molecule TIR-domain-containing adaptor-inducing interferon β (TRIF) in the response to L. interrogans has not been previously determined. In the present study, TRIF was found to play an important role during leptospiral infection. Following challenge with L. interrogans, Trif(-/-) mice exhibited delayed weight gain compared to wild-type mice. Moreover, Trif(-/-) mice exhibited an increase in L. interrogans burden in the kidneys, lungs, and blood at early time points (less than 7days post infection). Multiple components of the innate immune responses were dampened in response to leptospiral infection including transcription and production of cytokines, and the humoral response, which suggested that TRIF contributes to expression and production of cytokines important for the host defense against L. interrogans.}, number={9}, journal={IMMUNOBIOLOGY}, author={Jayaraman, Priya A. and Devlin, Amy A. and Miller, Jennifer C. and Scholle, Frank}, year={2016}, month={Sep}, pages={964–974} }
 @article{dumont_devlin_truempy_miller_singh_2015, title={No Evidence that Infection Alters Global Recombination Rate in House Mice}, volume={10}, ISSN={["1932-6203"]}, DOI={10.1371/journal.pone.0142266}, abstractNote={Recombination rate is a complex trait, with genetic and environmental factors shaping observed patterns of variation. Although recent studies have begun to unravel the genetic basis of recombination rate differences between organisms, less attention has focused on the environmental determinants of crossover rates. Here, we test the effect of one ubiquitous environmental pressure–bacterial infection–on global recombination frequency in mammals. We applied MLH1 mapping to assay global crossover rates in male mice infected with the pathogenic bacterium Borrelia burgdorferi, the causative agent of Lyme Disease, and uninfected control animals. Despite ample statistical power to identify biologically relevant differences between infected and uninfected animals, we find no evidence for a global recombination rate response to bacterial infection. Moreover, broad-scale patterns of crossover distribution, including the number of achiasmate bivalents, are not affected by infection status. Although pathogen exposure can plastically increase recombination in some species, our findings suggest that recombination rates in house mice may be resilient to at least some forms of infection stress. This negative result motivates future experiments with alternative house mouse pathogens to evaluate the generality of this conclusion.}, number={11}, journal={PLoS One}, author={Dumont, Beth L. and Devlin, Amy A. and Truempy, Dana M. and Miller, Jennifer C. and Singh, Nadia D.}, year={2015}, month={Nov} }