Toll‐like Receptor Signaling and Chemokine Receptor Expression Influence the Severity of Urinary Tract Infection

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Abstract
Urinary tract infections (UTIs) vary in pathogenesis and severity. After their ascent into the urinary tract, bacteria may establish asymptomatic bacteriuria (ABU), cause acute cystitis, or cause acute pyelonephritis. Research during the last few decades has established that the site of infection and the disease severity are influenced by bacterial virulence. In the 1940s, hemolysin was shown to identify Escherichia coli that cause extraintestinal infections [1]. “Uropathogenic” E. coli strains were later shown to belong to a restricted set of serotypes or clones [2], and acute pyelonephritis and ABU strains were shown to differ in surface antigen repertoire [3]. Studies in the 1970s started to involve host cell interactions with attachment to the urinary tract mucosa [4]. We proposed that the disease severity was a direct result of bacterial virulence and that tissue attachment is a first critical step. The special virulence of the uropathogenic clones has subsequently been shown to include numerous virulence factors encoded on the pathogenicity islands (see Middendorf et al., this issue)