Scanning Electron Microscopy of Human Bladder Mucosa in Acute and Chronic Urinary Tract Infection

Elliott, T. S. J.; Slack, R. C. B.; Bishop, M. C.

doi:10.1111/j.1464-410x.1984.tb07160.x

Cited by 30 publications

(10 citation statements)

References 10 publications

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“…This exfoliative process may not be entirely advantageous to the host, since shedding of uroepithelial cells will expose underlying tissue to bacteria that have escaped elimination. Internalization of bacteria by epithelial cells has been demonstrated in both the normal and disrupted uroepithelium (16,17,26,40). In fact, this internalization may give the pathogen access to a protected niche replete with nutrients.…”

Section: Discussionmentioning

confidence: 99%

“…Desquamation of uroepithelial cells to which bacteria have attached and the subsequent elimination of these cells during urination is considered to be an innate host defense mechanism (26,46). Indeed, this exfoliative response has been observed in humans with acute or chronic UTIs and in experimental UTI models with mice and rats (16,17,26,40,46). This exfoliative process may not be entirely advantageous to the host, since shedding of uroepithelial cells will expose underlying tissue to bacteria that have escaped elimination.…”

Section: Discussionmentioning

confidence: 99%

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Cytotoxic Necrotizing Factor Type 1 of Uropathogenic Escherichia coli Kills Cultured Human Uroepithelial 5637 Cells by an Apoptotic Mechanism

2000

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Pathogenic Escherichia coli associated with urinary tract infections (UTIs) in otherwise healthy individuals frequently produce cytotoxic necrotizing factor type 1 (CNF1), a member of the family of bacterial toxins that target the Rho family of small GTP-binding proteins. To gain insight into the function of CNF1 in the development of E. coli-mediated UTIs, we examined the effects of CNF1 intoxication on a panel of human cell lines derived from physiologically relevant sites (bladder, ureters, and kidneys). We identified one uroepithelial cell line that exhibited a distinctly different CNF1 intoxication phenotype from the prototypic one of multinucleation without cell death that is seen when HEp-2 or other epithelial cells are treated with CNF1. The 5637 bladder cell line detached from the growth surface within 72 h of CNF1 intoxication, a finding that suggested frank cytotoxicity. To determine the basis for the unexpected toxic effect of CNF1 on 5637 cells, we compared the degree of toxin binding, actin fiber formation, and Rho modification with those CNF1-induced events in HEp-2 cells. We found no apparent difference in the amount of CNF1 bound to 5637 cells and HEp-2 cells. Moreover, CNF1 modified Rho, in vivo and in vitro, in both cell types. In contrast, one of the classic responses to CNF1 in HEp-2 and other epithelial cell lines, the formation of actin stress fibers, was markedly absent in 5637 cells. Indeed, actin stress fiber induction by CNF1 did not occur in any of the other human bladder cell lines that we tested (J82, SV-HUC-1, or T24). Furthermore, the appearance of lamellipodia and filopodia in 5637 cells suggested that CNF1 activated the Cdc42 and Rac proteins. Finally, apoptosis was observed in CNF1-intoxicated 5637 cells. If our results with 5637 cells reflect the interaction of CNF1 with the transitional uroepithelium in the human bladder, then CNF1 may be involved in the exfoliative process that occurs in that organ after infection with uropathogenic E. coli.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Cytotoxic Necrotizing Factor Type 1 of Uropathogenic Escherichia coli Kills Cultured Human Uroepithelial 5637 Cells by an Apoptotic Mechanism

2000

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“…85-91], (5) Experimental intravesical instillation of hydro chloric acid [61][62][63][64] or protamine [65], claimed to create a leaky urothelium by selectively removing its GAG layer, in reality destroys the umbrella cells or even the entire urothelium [92. 93: Elbadawi and Theobald, to be pub lished], (6) It seems that the ultrastructure of surface 'mucinous' coat correlates with the topography of the urothelial surface rather than any specific bladder disease [94], The GAG layer tends to be thicker on a microvillous surface due to rapid cell turnover [41,42,94], Breaches in the GAG layer appear to be a manifestation of natural wear and tear [41] and have been observed in human urinary tract infection [44] and in rats with experimental cystitis [95], (7) No difference in ultrastructure of the GAG layer was found between normal urothelium and that in IC [41. 74],…”

Section: Discussionmentioning

confidence: 99%

Distinctive Ultrastructural Pathology of Nonulcerative Interstitial Cystitis

Jk²

1996

Urol Int

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Ultrastructural study of the bladder in interstitial cystitis has, so far, been limited, mainly to the urothelium. The present study was conducted first to study in detail the ultrastructural features of all tissue components of the bladder wall in nonulcerative interstitial cystitis and second to derive clues from the observed changes to pathogenesis of the disease. Endoscopic biopsies of urothelium with attached suburothelium, and muscularis, were obtained from both lesional and nonlesional areas in 5 female patients with unequivocal clinical diagnosis of interstitial cystitis. The specimens were processed for electron microscopic study by standard methods and subjected to comprehensive ultrastructural study of urothelium, suburothelium, detrusor muscle cells, intrinsic blood vessels, and intrinsic nerves. A distinctive combination of peculiar muscle cell profiles, injury of intrinsic vessels and nerves in muscularis and suburothelium, and discohesive urothelium was observed in lesional and less markedly in nonlesional samples of all specimens. Marked edema of various tissue elements and cells appeared to be a common denominator of many observed changes. Edema of muscle cells resulted in characteristic querciphylloid profiles, so designated because of peripheral bosselation of cell sarcoplasm with a lobed perimeter resembling that of an oak leaf. Urothelial changes disrupted the true permeability barrier, consisting of asymmetric unit membrane and triple epithelial junctions of surface (umbrella) cells. Vascular lesions included endothelial cell injury and suggested sluggishness of intrinsic microcirculation. Neural changes included a combination of degenerative and regenerative features, some expressing neural plasticity. The observed ultrastructural changes appear to be sufficiently distinctive to be diagnostic in specimens submitted for pathologic confirmation of nonulcerative interstitial cystitis. The changes do not support a primary pathogenetic role of mast cells or a selectively deficient glycosaminoglycan layer. They do suggest, however, a pathogenesis based on a potentially self-perpetuating process of neurogenic inflammation that can trigger a biologically potent cascade of events, including a leaky urothelium and mast cell activation. As proposed, neurogenic inflammation consolidates various proposals advanced as the pathogenesis of interstitial cystitis and can readily accommodate infectious, immunologic, and autoimmunologic mechanisms as factors that contribute to development or chronicity of the disease.

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“…The question is: might certain bacteria survive and possibly thrive within bladder epithelial cells or interstitium? Human data exist [29] suggesting that even well-recognized uropathogens may be viable and associated with the epithelium while the urine is sterile.…”

Section: Discussionmentioning

confidence: 99%

Different clinical presentation of interstitial cystitis syndrome

Porru

Politano

Gerardini

et al. 2004

International Urogynecology Journal and Pelvic Floor Dysfunctio

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The aim of the study was to examine how interstitial cystitis (IC) initiates its clinical course, which changes as the disease progresses from the initial phase to its full clinical manifestation. Patients diagnosed with IC between 1998 and 2003 in our department were evaluated and reviewed regularly. The exact onset of urinary symptoms was recorded. Diagnosis of IC was made by National Institute of Diabetes and Digestive and Kidney Disease (NIDDK) criteria when clinical suspicion of IC was present. The study group included 30 female patients who were 27-69 years old when diagnosis was made. Mean age was 46.7. Seventy percent of patients had only one symptom at onset. The most frequent initial diagnosis was urinary tract infection (UTI). A condition of recurrent bacterial UTIs, with subsequent persistence of symptoms and negative cultures, could be detected as a harbinger of IC in 60% of our patient group. IC may manifest initially with a single symptom in its early stage, when diagnosis is perhaps less easy, but adequate and effective treatment can still be offered to the patient.

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Scanning Electron Microscopy of Human Bladder Mucosa in Acute and Chronic Urinary Tract Infection

Cited by 30 publications

References 10 publications

Cytotoxic Necrotizing Factor Type 1 of Uropathogenic Escherichia coli Kills Cultured Human Uroepithelial 5637 Cells by an Apoptotic Mechanism

Cytotoxic Necrotizing Factor Type 1 of Uropathogenic Escherichia coli Kills Cultured Human Uroepithelial 5637 Cells by an Apoptotic Mechanism

Distinctive Ultrastructural Pathology of Nonulcerative Interstitial Cystitis

Different clinical presentation of interstitial cystitis syndrome

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