Establishment of a Mouse Model of Cystitis and Roles of Type 1 Fimbriated <i>Escherichia coli</i> in Its Pathogenesis

Liao, Jie; Tomochika, Ken Ichi; Watanabe, Sadahiro; Kanemasa, Yasuhiro

doi:10.1111/j.1348-0421.1992.tb01662.x

Cited by 9 publications

(4 citation statements)

References 20 publications

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“…Although others have assessed the interaction of E. coli strains and mouse bladder (1,5,8,21) or the development of cystitis and pyelonephritis following experimental challenge of mice or nonhuman primates with E. coli (16,31,32), this is the first study to assess differences between the uropathogenicities of pyelonephritis and cystitis strains of E. coli in an animal model of UTI. We chose to use the transurethrally challenged mouse model which was originally described by Hagberg et al (9), who documented that a P-fimbria-expressing strain colonized the kidney better than P-fimbria-negative strains.…”

Section: Discussionmentioning

confidence: 99%

Comparison of Escherichia Coli Strains Recovered From Human Cystitis and Pyelonephritis Infections in Transurethrally Challenged Mice

et al. 1999

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Urinary tract infection, most frequently caused by Escherichia coli, is one of the most common bacterial infections in humans. A vast amount of literature regarding the mechanisms through which E. coli induces pyelonephritis has accumulated. Although cystitis accounts for 95% of visits to physicians for symptoms of urinary tract infections, few in vivo studies have investigated possible differences between E. coli recovered from patients with clinical symptoms of cystitis and that from patients with symptoms of pyelonephritis. Epidemiological studies indicate that cystitis-associated strains appear to differ from pyelonephritis-associated strains in elaboration of some putative virulence factors. With transurethrally challenged mice we studied possible differences using three each of the most virulent pyelonephritis and cystitis E. coli strains in our collection. The results indicate that cystitis strains colonize the bladder more rapidly than do pyelonephritis strains, while the rates of kidney colonization are similar. Cystitis strains colonize the bladder in higher numbers, induce more pronounced histologic changes in the bladder, and are more rapidly eliminated from the mouse urinary tract than pyelonephritis strains. These results provide evidence that cystitis strains differ from pyelonephritis strains in this model, that this model is useful for the study of the uropathogenicity of cystitis strains, and that it would be unwise to use pyelonephritis strains to study putative virulence factors important in the development of cystitis.Although the bladder, particularly in women, is often exposed to bacteria and although urine generally supports bacterial growth, the combined effects of bladder emptying by urination and an intrinsic defense mechanism associated with bladder epithelium assist in resisting bacterial infection of the bladder (4, 28, 29). However, a breach of natural bladder defense mechanisms resulting from anatomical abnormalities of the urinary tract or, more commonly, virulence factors expressed by the colonizing bacteria results in urinary tract infection (UTI). Symptomatic UTI is manifest in two syndromes. One is acute pyelonephritis clinically identified by flank pain and fever and generally perceived as being a kidney infection. The second is cystitis, characterized by dysuria and increased frequency and urgency of urination, which is generally perceived to be a bladder infection and accounts for 95% of all visits to physicians for UTIs (7).In the normal urinary tract, most UTIs are caused by Escherichia coli. Studies on the uropathogenicity of E. coli have focused primarily on the development of pyelonephritis. Epidemiologic studies have implicated adhesins, particularly P fimbriae, and other factors, such as hemolysin, in the development of acute pyelonephritis; some of these have been confirmed to be virulence factors by in vitro and in vivo studies (9,10,(18)(19)(20). Only recently have epidemiologic studies begun to focus on cystitis, the more frequent UTI syndrome. Although some put...

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Section: Discussionmentioning

confidence: 99%

Comparison of Escherichia Coli Strains Recovered From Human Cystitis and Pyelonephritis Infections in Transurethrally Challenged Mice

et al. 1999

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“…Liao et al [19] reported that removal of superficial cells was essential for the adherence of type 1 fimbriated E. coli to the bladder epithelia. In contrast, our results showed that the superficial cells in the infected bladders were not desquamated, but stained strongly or interme diately positive for almost all lectins, especially for Con A.…”

Section: Discussionmentioning

confidence: 99%

Increase in Lectin Binding Sites on Epithelial Cells by Chronic Bladder Infection in Rats

Nakagawa

Kitami²,

Watanabe³

et al. 1996

Urol Int

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Using lectin histochemistry we assessed whether chronic bladder infection modifies carbohydrate residues of glycoconjugates on uroepithelial cells in rats. The bladder infection was produced by implanting a knotted silk thread with Escherichia coli into the bladder. One or 4 weeks after the implantation the bladder was excised, incubated with sixteen biotinylated lectins and stained. The bladder epithelia as a whole stained more strongly positive for eight lectins in the infected rats than in the control rats having a sterile silk thread in the bladder. In the infected rats, the superficial epithelial layer that stained negative for Arachis hypogaea (PNA) in the controls became strongly positive for PNA, whereas the middle and deep epithelial layers increased in staining for Canavalia ensiformis and six other lectins. These results indicate that chronic bladder infection increases carbohydrate residues on uroepithelial cells and may facilitate bacterial adherence to uroepithelial cells.

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“…In some experiments, various proton pump inhibitors in 20 ul PBS were injected into the bladder lumen via the urethra [12], and then time courses of the urinary pH were followed.…”

Section: Measurement Of Urinary Phmentioning

confidence: 99%

Vacuolar‐type H⁺‐ATPase in mouse bladder epithelium is responsible for urinary acidification

et al. 1997

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Establishment of a Mouse Model of Cystitis and Roles of Type 1 Fimbriated Escherichia coli in Its Pathogenesis

Cited by 9 publications

References 20 publications

Comparison of Escherichia Coli Strains Recovered From Human Cystitis and Pyelonephritis Infections in Transurethrally Challenged Mice

Comparison of Escherichia Coli Strains Recovered From Human Cystitis and Pyelonephritis Infections in Transurethrally Challenged Mice

Increase in Lectin Binding Sites on Epithelial Cells by Chronic Bladder Infection in Rats

Vacuolar‐type H⁺‐ATPase in mouse bladder epithelium is responsible for urinary acidification

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Establishment of a Mouse Model of Cystitis and Roles of Type 1 Fimbriated Escherichia coli in Its Pathogenesis

Cited by 9 publications

References 20 publications

Comparison of Escherichia Coli Strains Recovered From Human Cystitis and Pyelonephritis Infections in Transurethrally Challenged Mice

Comparison of Escherichia Coli Strains Recovered From Human Cystitis and Pyelonephritis Infections in Transurethrally Challenged Mice

Increase in Lectin Binding Sites on Epithelial Cells by Chronic Bladder Infection in Rats

Vacuolar‐type H+‐ATPase in mouse bladder epithelium is responsible for urinary acidification

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Vacuolar‐type H⁺‐ATPase in mouse bladder epithelium is responsible for urinary acidification