@inbook{ae901242-b065-4cd3-b981-6455cbf85390,
  abstract     = {{<p>Urinary tract infections offer an important and highly relevant model to understand innate immune-mediated protection against mucosal infection and innate immune genetics of susceptibility, including promoter polymorphisms reducing Toll-like receptor (TLR) and interferon regulatory factor expression. Whereas virulent Escherichia coli causes severe, potentially life-threatening disease by breaking the inertia of the mucosal barrier, the most common outcome of bacteriuria is an asymptomatic carrier state (ABU) resembling commensalism at other mucosal sites. Pathogens gain a short-term advantage by expressing virulence factors that dysregulate a range of innate signaling pathways and effector functions, including molecules that inactivate TLR signaling. Genome sequencing has revealed that ABU strains, in contrast, have evolved by reductive evolution with a loss of virulence genes and gain of a new class of host RNA polymerase II suppressive activity. These extremes illustrate aspects of "good" versus "bad" inflammation, pathology versus symbiosis. Novel therapeutic approaches based on these molecular interactions are discussed.</p>}},
  author       = {{Ambite, Ines and Lutay, Nataliya and Godaly, Gabriela and Svanborg, Catharina}},
  booktitle    = {{Mucosal Immunology}},
  isbn         = {{9780124159754}},
  keywords     = {{Host genetics; Innate immunity; Mucosal immunity; Pathogen specificity; Therapy; Urinary tract infection}},
  language     = {{eng}},
  month        = {{04}},
  pages        = {{2039--2058}},
  publisher    = {{Mosby-Elsevier}},
  title        = {{Urinary Tract Infections and the Mucosal Immune System}},
  url          = {{http://dx.doi.org/10.1016/B978-0-12-415847-4.00106-3}},
  doi          = {{10.1016/B978-0-12-415847-4.00106-3}},
  volume       = {{2}},
  year         = {{2015}},
}