Blocking adherence of uropathogenic Escherichia coli isolate to HEP-2 cells and bladder of mice in the presence of antibody against p-fimbriae.

Presence of fimbriae on Escherichia coli isolated from the urine of patients with urinary tract infection was related to the ability of the bacteria to attach to human uroepithelial cells. One of the 50 isolates that expresses high MRHA p-fimbriae, selected and antibody against p-fimbriae from it, showed blocking of attachment of bacteria to HEP-2 cell in 1:1024 titer. Also, 1:512 titer of this antiserum to blocking of attachment in bladder tissue of mice is significant.

Bidhendi SM ，Sattari M ，Pourbakhsh SA ，Mobarez A ，Vandyousefi J ，Khaki P ，Heidari MH ，Kazemnejad A ... -  《BIOLOGICALS》

Expression of type 1 and P fimbriae in situ and localisation of a uropathogenic Escherichia coli strain in the murine bladder and kidney.

:Adhesion is an important aspect of bacterial colonisation and induction of human disease. Escherichia coli which infects and causes disease of the urinary tract expresses several adherence factors including type 1 and P fimbriae. Their expression has been implicated in the virulence of E. coli strains infecting the urinary tract, however, the evidence for the expression of these fimbriae in situ has been implied rather than proven. Here we describe in situ detection of E. coli and of fimbrial expression in urinary tract tissue. Kidneys and bladders were isolated from mice infected with the uropathogenic isolate E. coli AD110. The tissue was sectioned and subjected to DNA-rRNA hybridization and indirect immunofluorescent staining with antibodies against type 1 and P fimbriae. Sections of both kidney and bladder stained positive for bacterial cells using a Cy3-labelled E. coli-specific rRNA probe. The same cells in these sections also stained positive for type 1 or P fimbriae using fluorescein-labelled antibodies. Tissue taken from several different time points (2, 6, and 24 hours post infection) showed the presence of bacterial cells which stained positive for fimbrial expression. Bacteria in kidney and bladder sections were observed either as individual cells associated with the mucosa or as members of microcolonies.

Connell H ，Poulsen LK ，Klemm P 《INTERNATIONAL JOURNAL OF MEDICAL MICROBIOLOGY》

Systemic immunization with conserved pilus-associated adhesins protects against mucosal infections.

Colonization and infection of the bladder mucosa by Escherichia coli, the major uropathogenic organism, is dependent on the expression of pilus organelles. Type 1 pili are expressed by the majority of E. coli strains derived from patients with cystitis and pyelonephritis. FimH is the adhesin protein located at the distal tip of the heteropolymeric type-1 pilus which mediates binding to bladder cells through mannose receptors. We have shown that humoral antibody raised against two forms of purified FimH adhesin inhibited 94% (49/52) of E. coli UTI clinical isolates from binding to bladder tissue in vitro. Animals immunized with FimH-containing vaccines by a systemic route reduced colonization of the bladder mucosa in vivo in a murine cystitis model by > 99%. IgG antibody to FimH was detected in urinary samples obtained from immunized, protected mice. Passive systemic administration of immune sera from FimH-inoculated mice to naive animals also resulted in reduced colonization of bladder mucosa by uropathogenic E. coli. These studies demonstrate that systemic immunization with an anti-bacterial vaccine targeting a highly conserved adhesin on uropathogenic E. coli can induce IgG-mediated protection at a mucosal surface and may be a means of preventing recurrent and acute infections of the urogenital tract mucosa.

Palaszynski S ，Pinkner J ，Leath S ，Barren P ，Auguste CG ，Burlein J ，Hultgren S ，Langermann S ... -  《-》

Intracellular bacterial biofilm-like pods in urinary tract infections.

Escherichia coli entry into the bladder is met with potent innate defenses, including neutrophil influx and epithelial exfoliation. Bacterial subversion of innate responses involves invasion into bladder superficial cells. We discovered that the intracellular bacteria matured into biofilms, creating pod-like bulges on the bladder surface. Pods contained bacteria encased in a polysaccharide-rich matrix surrounded by a protective shell of uroplakin. Within the biofilm, bacterial structures interacted extensively with the surrounding matrix, and biofilm associated factors had regional variation in expression. The discovery of intracellular biofilm-like pods explains how bladder infections can persist in the face of robust host defenses.

Anderson GG ，Palermo JJ ，Schilling JD ，Roth R ，Heuser J ，Hultgren SJ ... -  《-》

Microbiology. Pods invade infected bladders.

Ferber D 《-》