The spirochete Borrelia burgdorferi causes Lyme disease, which is transmitted to humans when its vector, the deer tick, takes a blood meal. When B. burgdorferi is in the gut of the tick, its outer surface protein A (OspA) is expressed at high levels. Once it has been transmitted to a human, OspA production diminishes. However, to complete its infection cycle and return to the tick, B. burgdorferi cells must increase OspA synthesis. Microbiologists wanted to determine how the spirochete senses the presence of a feeding tick and thus resumes high levels of OspA production. It was discovered that B. burgdorferi specifically binds the host neuroendocrine stress hormones epinephrine and norepinephrine. This enables the microbe to detect the presence of a tick, which results in upregulation of OspA.
Discuss the role of coevolution in the development of B. burgdorferi’s ability to sense and respond to these host compounds. How would you show that among all the mediators of inflammation at the site of a tick bite, the spirochete responds specifically to epinephrine and norepinephrine? Your answer should include some carefully considered control experiments.
Read the original paper: Schekelhoff, M. R., et al. 2007. Borrelia burgdorferi intercepts host hormonal signals to regulate expression of outer surface protein A. Proc. Natl. Acad. Sci. USA 104:7247–52.
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Prescott's Microbiology
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