My laboratory is interested in understanding how Borrelia burgdorferi, the causative agent of Lyme disease, counteracts oxidative and nitrosative stress upon transmission to the mammalian host. The ability of B. burgdorferi to colonize mammals is dependent on its ability to rapidly alter gene expression in response to highly disparate environmental signals following transmission from infected ticks. Furthermore, this bacterium has a very limited number of genes involved in counteracting oxidative and nitrosative stress, with one single superoxide dismutase (sodA) and no typical catalases and peroxidases. We have demonstrated that the sodA gene is essential for infectivity in the mouse model. Therefore, our goal is to further analyze the molecular mechanisms adopted by B. burgdorferi to combat reactive oxygen and nitrogen species, and to dissect critical physiological responses against these stressors in the processes facilitating colonization of the mammalian hosts. We are also interested in a new family of membrane proteins, known as von Willebrand factor A containing proteins (VWFA), which have been described in other bacterial pathogens as potential adhesines. Our main goal is to understand the topology, insertion in the membranes and function of these proteins in B. burgdorferi during transmission from the infected tick to the mammalian host.
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