Concrement formation in the urinary bladder in rats inoculated with Ureaplasma urealyticum

Grenabo, L.; Brorson, John‐Erik; Hedelin, Hans; Pettersson, S.

doi:10.1007/bf00261823

Cited by 16 publications

(11 citation statements)

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“…time points. Based on these results, we surmise that invasive colonization of the bladder triggers chronic inflammation and immune dysregulation, which may be critical to struvite formation.Struvite or infection stones form as a result of complicated urinary tract infections (UTI) caused by urease-producing bacteria such as Proteus, Klebsiella, Serratia, and Ureaplasma species (5,8,9,17). Bacterial urease breaks down urea into ammonia, resulting in urine's becoming supersaturated with ammonia.…”

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confidence: 99%

Complicated Urinary Tract Infection Is Associated with Uroepithelial Expression of Proinflammatory Protein S100A8

et al. 2009

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F344 rats chronically infected with Ureaplasma parvum develop two distinct profiles: asymptomatic urinary tract infection (UTI) and UTI complicated by struvite urolithiasis. To identify factors that affect disease outcome, we characterized the temporal host immune response during infection by histopathologic analysis and in situ localization of U. parvum. We also used differential quantitative proteomics to identify distinguishing host cellular responses associated with complicated UTI. In animals in which microbial colonization was limited to the mucosal surface, inflammation was indistinguishable from that which occurred in shaminoculated controls, and the inflammation resolved by 72 h postinoculation (p.i.) in both groups. However, inflammation persisted in animals with microbial colonization that extended into the deeper layers of the submucosa. Proteome profiling showed that bladder tissues from animals with complicated UTIs had significant increases (P < 0.01) in proteins involved in apoptosis, oxidative stress, and inflammation. Animals with complicated UTIs (2 weeks p.i.) had the highest concentrations of the proinflammatory protein S100A8 (P < 0.005) in bladder tissues, and the levels of S100A8 positively correlated with those of proinflammatory cytokines GRO/KC (P < 0.003) and interleukin-1␣ (P < 0.03) in urine. The bladder uroepithelium was a prominent cell source of S100A8-S100A9 in animals with complicated UTIs (2 weeks p.i.), which was not detected in animals with asymptomatic UTIs (2 weeks p.i.) or in any bladder tissues harvested at earlier p.i. time points. Based on these results, we surmise that invasive colonization of the bladder triggers chronic inflammation and immune dysregulation, which may be critical to struvite formation.Struvite or infection stones form as a result of complicated urinary tract infections (UTI) caused by urease-producing bacteria such as Proteus, Klebsiella, Serratia, and Ureaplasma species (5,8,9,17). Bacterial urease breaks down urea into ammonia, resulting in urine's becoming supersaturated with ammonia. When this occurs, the urine pH rises and the solubility of magnesium ammonium phosphate decreases, leading to crystal deposition and stone formation. Infection is always an underlying cause of struvite urolithiasis (5, 9). Therefore, it is not surprising that known predisposing factors such as renal tubular acidosis, neurogenic bladder, urinary tract obstructions, and chronic use of indwelling catheters (5, 9) are related to elements that increase patient susceptibility to UTI. Although infections usually induce an inflammatory response in the host, to our knowledge, the role of the host immune response as a potential predisposing factor in struvite urolithiasis has not been evaluated or considered to be important in disease pathogenesis. We present data suggesting that the host immune response plays a critical role in the development of struvite stones and that the proinflammatory protein S100A8-S100A9 may play a critical role in the chronic inflammation and immune...

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Complicated Urinary Tract Infection Is Associated with Uroepithelial Expression of Proinflammatory Protein S100A8

et al. 2009

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“…Although Ureaplasma is not a natural pathogen of rodents, experimental infection of the rodent urinary tract with Ureaplasma has been established by inoculation into the bladder and/or renal pelvis (10,22,23,27,28). Experimental infection in different rat strains produces a wide spectrum of disease ranging from mild inflammation to predominantly hyperplastic lesions of the bladder with varying degrees of pyelonephritis and urolithiasis (10,22,23,27,29). These studies were done under different conditions with different isolates of Ureaplasma; therefore, direct comparisons cannot be made.…”

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Rat Strains Differ in Susceptibility to Ureaplasma parvum -Induced Urinary Tract Infection and Struvite Stone Formation

et al. 2006

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Individuals with struvite uroliths are susceptible to recurrent urinary tract infections (UTI), sepsis, and renal disease. Unfortunately, little is known about the host-specific factors that predispose to this disease. In order to develop a rodent model that can address this problem, we inoculated female Fischer 344 (F344), Lewis (LEW), Sprague-Dawley (SD), and Wistar (WIS) rats with a host-adapted strain of Ureaplasma parvum. Animals were necropsied at 2 weeks postinoculation; 100% of F344, 42% of SD, 10% of LEW, and 10% of WIS rats remained infected. Severe bladder lesions and struvite calculi were seen in 64% of F344 rats; in other rat strains, bladder lesions were mild or absent. F344 rats with struvite uroliths had the highest urinary levels of proinflammatory cytokines, such as GRO/KC, interleukin-1␣ (IL-1␣), and IL-1␤. F344 rats without struvite stones at necropsy had milder bladder lesions and significantly lower urinary levels of proinflammatory cytokines but a more prominent inflammatory response than did other rat strains. Based on our results, struvite stone formation is linked to a robust inflammatory response that does not resolve UTI but instead promotes damage to surrounding tissues.Although struvite calculi constitute only 2 to 3% of stones that are analyzed, they create greater clinical complications, such as sepsis and renal disease (30), than any other stone type. Not all factors that contribute to struvite stone formation are known, but urinary tract infections (UTI) are usually a predisposing factor. Infections with urease-producing bacteria, such as Klebsiella, Proteus, Pseudomonas, and Ureaplasma, significantly increase the risk of struvite formation due to increases in urine pH and direct damage of the uroepithelium by ammonia (13, 29).Host-specific factors also increase the risk of struvite formation during a UTI episode. Obvious examples of host-specific factors are anatomic anomalies of the urogenital tract that disrupt the capacity to void urine (13, 29). However, in most patients a predisposing factor cannot be identified, and the underlying cause of struvite stone formation remains unclear. Since UTI is a prerequisite for struvite stone formation, risk factors for UTI also need to be considered. In women, colonization of the vagina with potential uropathogens combined with impaired host defense mechanisms increases the risk of UTI (7,32,38). In addition, genetic factors have been postulated to play a role in susceptibility to UTI (37).Although ureaplasmas are not the only urease-producing bacteria known to cause struvite calculi (11,12,14), they are uniquely considered opportunistic pathogens because they can be readily isolated from the lower urogenital tract of healthy humans as well as individuals with disease (26, 39). Epidemiological studies show that women have much higher Ureaplasma colonization rates (5) as well as higher rates of infection-induced calculi that are culture positive for Ureaplasma (19) than do men. Since most diseases caused by mollicutes are influenced by a...

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“…One urease inhibitor, fluorofamide, will inhibit the growth of Ureaplasma but not Mycoplasma species [22]. Clinical struvite stone disease can clearly be produced by Ureaplasma organisms [23], and it is likely that many seemingly culture-negative cases are caused by these organisms [24]. Since long-term suppression with tetracycline may be possible, the distinction is important [25].…”

Section: Bacteriologymentioning

confidence: 99%

Struvite Stones

Rodman¹

1998

Nephron

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Struvite stones constitute only about 2–3% of the stones reaching the laboratory for analysis, but the clinical problems they create including sepsis and even renal demise are greater than with any other stone type. This article reviews the evidence that bacterial urease, usually from a Proteus species, is responsible for the chemical changes in urine which result in struvite formation. Available urease inhibitors and other forms of medical management of patients with these stones are discussed. A patient with struvite stones should be assumed to have a progressive disease which cannot be ignored. Even after seemingly successful elimination of stones with lithotripsy and/or percutaneous nephrolithotomy, careful medical follow-up is critical. The medical profession is probably underutilizing postprocedure hemiacidrin irrigation because of shortsighted financial considerations. Primary-care physicians need to be educated in the importance of aggressive management of Proteus and other urea-splitting infections.

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Concrement formation in the urinary bladder in rats inoculated with Ureaplasma urealyticum

Cited by 16 publications

References 11 publications

Complicated Urinary Tract Infection Is Associated with Uroepithelial Expression of Proinflammatory Protein S100A8

Complicated Urinary Tract Infection Is Associated with Uroepithelial Expression of Proinflammatory Protein S100A8

Rat Strains Differ in Susceptibility to Ureaplasma parvum -Induced Urinary Tract Infection and Struvite Stone Formation

Struvite Stones

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