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4Q * 3P * M Poblocki, Dan. The Book of Bad Things. Scholastic, 2014. 256p. $16.99. 978-0-545-64553-9. The world is full of bad things, like cramped apartments in the city [...]

ABSTRACTHelicobacter pyloripersistently colonizes the harsh and dynamic environment of the stomach in over one-half of the world's population and has been identified as a causal agent in a spectrum of pathologies that range from gastritis to invasive adenocarcinoma. The ferric uptake regulator (Fur) is one of the few regulatory proteins that has been identified in H. pylori. Fur regulates genes important for acid acclimation and oxidative stress and has been shown to be important for colonization of H. pyloriin both murine and Mongolian gerbil models of infection. To more thoroughly define the role of Fur in vivo, we conducted an extensive temporal analysis of the location of, competitive ability of, and resultant pathology induced by a Δfurstrain in the Mongolian gerbil model of infection and compared the results to results for its wild-type parent. We found that at the earliest time points postinfection, significantly more Δfurbacteria than wild-type bacteria were recovered. However, this trend was reversed by day 3, when there was significantly increased recovery of the wild-type strain. The increased recovery of the Δfurstrain at 1 day postinfection reflected increased recovery from both the corpus and the antrum of the stomach. When the wild-type strain was allowed to colonize first, the Δfurstrain was unable to compete for colonization at any time postinfection. However, when the Δfurstrain was allowed to colonize first, the wild type efficiently outcompeted the Δfurstrain only at early times postinfection. Finally, we demonstrated that there was a delay in the development and severity of inflammation and pathology of the Δfurstrain in the gastric mucosa even after comparable levels of colonization occurred. Together, these data indicate that H. pyloriFur is most important at early stages of infection and illustrate the importance of the ability of H. pylorito adapt to its constantly fluctuating environment when it is establishing infection, inflammation, and disease.