Host–pathogen checkpoints and population bottlenecks in persistent and intracellular uropathogenicEscherichia colibladder infection

Abstract

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 Escherichia 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 (IBCs), a process which requires type 1 pili. IBCs 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.

A comprehensive guide to pilus biogenesis in Gram-negative bacteria

“…The host receptors targeted by FimH include D-mannosylated receptors such as the uroplakins of the bladder, whereas PapG targets galabiose-containing glycosphingolipids which are primarily located on the kidney epithelium [37][38][39] . Therefore, the receptor specificity of the type 1 and P pilus lectin domains may contribute to the observed tropism towards the bladder and/or the kidney during the course of an infection, respectively 40 .…”

Antibiotics Resistance Profile of Uropathogens Isolated from Al Buraimi Hospital, Sultanate of Oman

“…In most cases uncomplicated UTIs affects those individuals who are salubrious and do not exhibit any structural or neurological urinary tract irregularities (Hooton, 2012;Nielubowicz & Mobley, 2010). These infections are divided into upper UTIs (pyelonephritis) and lower UTIs (cystitis) (Hannan et al, 2012;Hooton, 2012). Bacterial pathogens are perceived as the behind the cause of dispense symptoms, are treated with antibiotics ordinarily, in the case of primary care settings they account for nearly 95% of the antibiotic prescription for urinary tract infection (Ong, Kuyvenhoven, Van Dijk, & Verheij, 2008).…”

Molecular mechanism of bacterial type 1 and P pili assembly

“…These surface structures made of thousands of protein subunits (called pilins) are known to be essential for biofilm formation [2], and are particularly relevant to human health, because the tip proteins of such pili, called adhesins, are able to bind to specific host tissues. This adhesion step is crucial in the host colonization cycle by both Gram-positive and -negative bacterial pathogens (for review, refer to [3][4][5]). …”