Mechanisms and consequences of bladder cell invasion by uropathogenic Escherichia coli

Abstract

Strains of uropathogenic Escherichia coli (UPEC) are the major cause of urinary tract infections worldwide. Multiple studies over the past decade have called into question the dogmatic view that UPEC strains act as strictly extracellular pathogens. Rather, bacterial expression of filamentous adhesive organelles known as type 1 pili and Afa/Dr fibrils enable UPEC to invade host epithelial cells within the urinary tract. Entry into bladder epithelial cells provides UPEC with a protected niche where the bacteria can persist quiescently for long periods, unperturbed by host defences and protected from many antibiotic treatments. Alternately, internalized UPEC can rapidly multiply, forming large intracellular inclusions that can contain several thousand bacteria. Initial work aimed at defining the host and bacterial factors that modulate the entry, intracellular trafficking, and eventual resurgence of UPEC suggests a high degree of host-pathogen crosstalk. Targeted disruption of these processes may provide a novel means to prevent and treat recurrent, relapsing and chronic infections within the urinary tract.

Detection of virulence genes, phylogenetic group and antibiotic resistance of uropathogenic Escherichia coli in Mongolia

“…UTIs are one of the inflammatory diseases produced by high multiplication of many pathogens in the urinary apparatus, resulting in alterations in the function of the urinary tract and kidneys [2]. UTI is particularly a major problem for females; nearly 50% of all women will experience at least one UTI in their lifetime and, of those, about 25% will have one or more recurrent infections [3]. In Mongolia, UTI status has not been described, but females between 20 and 40 years of age accounted for 60.3% of all patients with chronic pyelonephritis [4].…”

“…The interaction between UPEC and epithelial cells is a multifactorial and complex phenomenon which involves several adhesins produced according to the stage of infection, while adherence to epithelial cells is essential for successful colonization and establishment. The expression of other genes encoding virulence factors contributes to disease severity [3,7]. The genes in the pathogenicity islands may also be virulence associated and encode a variety of different virulence factors, such as adherence factors (e.g., type 1 and P fimbriae), toxins (e.g., hemolysin and cytotoxic necrotizing factor), secretion systems, and siderophores (e.g., aerobactin and yersinabactin) [8][9][10].…”

Strengths and Limitations of Model Systems for the Study of Urinary Tract Infections and Related Pathologies

“…One of the most frequently studied adhesins, which is expressed by nearly all UPEC isolates, is the type 1 pilus-associated protein FimH. This adhesin can bind a variety of mannose-containing host membrane glycoproteins as well as components of the extracellular matrix (51). Upon entering the bladder, UPEC encounters a thin glycosaminoglycan-rich glycocalyx that is in loose association with the terminally differentiated superficial umbrella cells that comprise the outer layer of the urothelium (52)(53)(54).…”

Genotypic analysis of Escherichia coli strains that cause urosepsis in the Aegean region

“…Sepsis, also known as systemic inflammatory response syndrome, is a serious clinical picture triggered by infection of the bloodstream (12,13). Urinary tract infections are common and as a result of inadequate treatment, the disease progresses, and more serious illnesses such as sepsis can occur (14,15).…”