
Host–pathogen checkpoints and population bottlenecks in persistent and intracellular uropathogenic E scherichia coli bladder infection
Author(s) -
Hannan Thomas J.,
Totsika Makrina,
Mansfield Kylie J.,
Moore Kate H.,
Schembri Mark A.,
Hultgren Scott J.
Publication year - 2012
Publication title -
fems microbiology reviews
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.91
H-Index - 212
eISSN - 1574-6976
pISSN - 0168-6445
DOI - 10.1111/j.1574-6976.2012.00339.x
Subject(s) - urothelium , biology , microbiology and biotechnology , pathogen , population , bacteriuria , immunology , chronic infection , escherichia coli , pilus , fimbria , urinary system , immune system , gene , medicine , genetics , environmental health , endocrinology
Bladder infections affect millions of people yearly, and recurrent symptomatic infections (cystitis) are very common. The rapid increase in infections caused by multidrug‐resistant uropathogens threatens to make recurrent cystitis an increasingly troubling public health concern. Uropathogenic E scherichia coli ( UPEC ) cause the vast majority of bladder infections. Upon entry into the lower urinary tract, UPEC face obstacles to colonization that constitute population bottlenecks, reducing diversity, and selecting for fit clones. A critical mucosal barrier to bladder infection is the epithelium (urothelium). UPEC bypass this barrier when they invade urothelial cells and form intracellular bacterial communities ( IBC s), a process which requires type 1 pili. IBC s are transient in nature, occurring primarily during acute infection. Chronic bladder infection is common and can be either latent, in the form of the quiescent intracellular reservoir ( QIR ), or active, in the form of asymptomatic bacteriuria ( ASB / ABU ) or chronic cystitis. In mice, the fate of bladder infection, QIR , ASB , or chronic cystitis, is determined within the first 24 h of infection and constitutes a putative host–pathogen mucosal checkpoint that contributes to susceptibility to recurrent cystitis. Knowledge of these checkpoints and bottlenecks is critical for our understanding of bladder infection and efforts to devise novel therapeutic strategies.