Urease induced calcium precipitation by Helicobacter species may initiate gallstone formation

Belzer, Clara; Kusters, JG; Kuipers, Ernst J.; Vliet, Arnoud H. M. van

doi:10.1136/gut.2006.098319

Cited by 52 publications

(35 citation statements)

References 9 publications

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“…are enzootic in mouse colonies worldwide, and colonize the distal intestine and bile canaliculi 14 . Interestingly, the human gastric pathogen H. pylori, and two urease-negative enterohepatic helicobacters are not able to promote cholesterol gallstone formation in this model 13,15,16 . Aside from the gallstone phenotype, the most notable findings in mice infected with cholelithogenic Helicobacter spp.…”

Section: Introductionmentioning

confidence: 75%

T-Cell Function Is Critical for Murine Cholesterol Gallstone Formation

Maurer

Rao

et al. 2007

Gastroenterology

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Section: Introductionmentioning

confidence: 75%

T-Cell Function Is Critical for Murine Cholesterol Gallstone Formation

Maurer

Rao

et al. 2007

Gastroenterology

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“…Interestingly, a follow-up study showed that urease-positive Helicobacter spp can precipitate calcium salts in vitro 144. The investigators of this study proposed that this activity might contribute, at least in part, to the ability of these organisms to promote cholesterol gallstones by inducing the formation of a calcium salt nidus, because monoinfection with urease-positive helicobacters or coinfection with at least one urease-positive helicobacter is necessary to induce cholesterol gallstones 16,144…”

Section: Role Of Infection Inflammation and The Immune System In Fomentioning

confidence: 98%

Roles of Infection, Inflammation, and the Immune System in Cholesterol Gallstone Formation

2009

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Cholesterol gallstone formation is a complex process mediated by genetic and environmental factors. Until recently, the role of the immune system in the pathogenesis of cholesterol gallstones was not considered a valid topic of research interest. This review collates and interprets an extensive body of basic literature, some of which is not customarily considered to be related to cholelithogenesis, describing the multiple facets of the immune system that appear to be involved in cholesterol cholelithogenesis. A thorough understanding of the immune interactions with biliary lipids and cholecystocytes should modify current views of the pathogenesis of cholesterol gallstones, promote further research on the pathways involved, and lead to novel diagnostic tools, treatments, and preventive measures.Bile is a complex aqueous colloidal system that is essential for a wide range of physiologic functions, including the excretion of lipids from the organism and intestinal fat absorption. 1,2 Bile is formed primarily in hepatic canaliculi, small (1-2 μm) spaces formed between the tight junctions of hepatocytes. It is composed of water, electrolytes, and a variety of lipid solutes dispersed in mixed micelles and vesicles including bile salts, phospholipids (>96% being mixed phosphatidylcholines), and cholesterol, as well as proteins and bilirubin conjugates. 3 Phospholipids and bile salts are essential for the removal from the organism of otherwise insoluble cholesterol molecules in an aqueous environment by solubilizing the sterol in mixed micelles, composed of the catabolic product bile salts, and unilamellar vesicles. [2][3][4] Bile is transported from the canaliculi along tubules of increasingly greater diameter until it egresses into the gut at the midduodenum. In health, about half the secreted bile is stored, concentrated, and slightly acidified in the gallbladder during the interdigestive interval. The gallbladder is connected to the biliary tree via the cystic duct, which functions simultaneously as a gallbladder filling and emptying conduit. 3 Alterations in the relative or absolute proportions of cholesterol, phospholipids, and bile salts can lead to phase separation of cholesterol from solution in bile. Most frequently these changes Address requests for reprints to: Kirk J. Maurer, DVM, PhD, Cornell Center for Animal Resources and Education, College of Veterinary Medicine, Cornell University, Ithaca, New York. e-mail: km429@cornell.edu; fax: (607) 253-3527. M.C.C. and J.G.F. contributed equally to this work. John P. Lynch and David C. Metz, Section EditorsThe authors disclose no conflicts. NIH Public Access Author ManuscriptGastroenterology. Author manuscript; available in PMC 2010 February 1. Published in final edited form as:Gastroenterology. NIH-PA Author ManuscriptNIH-PA Author Manuscript NIH-PA Author Manuscript result from excess secretion of cholesterol from the liver. [1][2][3] As the absolute cholesterol concentration increases, the excess cholesterol phase separates, forming unilamellar vesicle...

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“…Belzer et al postulated that the urease activity of bacteria in calcium precipitation leads to nucleation for gallstone formation (33). We have experimentally established the role of urease in calcium precipitation and slime activity of bacteria in stone solidification under in vitro conditions.…”

Section: Discussionmentioning

confidence: 85%

Urease Positive and Slime Producing Bacterial Activity: Results in Gallstone Precipitation and Solidification

Sharma

Sachan

Sharma

2013

Arch Clin Infect Dis

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Background: Bacteria are commonly isolated from gallstones. Presence of bacteria in gallstones might play a role in their formation. Objectives: We aimed to study different properties of isolates from gallstones and their relationship with the mechanism of gallstone formation. Patients and Methods:This study included 526 subjects. Gallstones and bile samples of the patients were cultured. Isolates were identified by different biochemical tests and examined for their β-glucuronidase activity, slime production and Urease activity. Biostatistical analyses were done to determine the relationship between the biliary bacterial factors and the types of gallstones. Role of Slime and urease activity in mechanism of gallstone formation were tested in vitro. Results: Overall, 94.77% of the gallstones were found to be infected, of which 85% of the cholesterol stones, 97% of pigmented stones and 100% of mixed stones showed the presence of bacterial isolates (P < 0.0001). β-glucuronidase activity was associated with isolates from pigmented or mixed stones and completely absent in cholesterol gallstones (P = 0.018). Urease activity was basically associated with cholesterol gallstones (P < 0.0001) while slime (P < 0.0001) activity was not specific for any single type of stone formation yet isolates of bile had a significant association with slime activity. In vitro analysis demonstrated that bacteria with urease activity are involved in CaCO 3 precipitation and slime-producing isolates solidify the precipitated CaCO 3 . Conclusions: β-glucuronidase activity is mainly responsible for pigmented gallstone formation. Urease activity was predicted to be involved in nucleation and slime production during solidification of gallstones, as observed during in vitro studies. Hence, presence of these bacterial factors may enhance gallstone formation.

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Urease induced calcium precipitation by Helicobacter species may initiate gallstone formation

Cited by 52 publications

References 9 publications

T-Cell Function Is Critical for Murine Cholesterol Gallstone Formation

T-Cell Function Is Critical for Murine Cholesterol Gallstone Formation

Roles of Infection, Inflammation, and the Immune System in Cholesterol Gallstone Formation

Urease Positive and Slime Producing Bacterial Activity: Results in Gallstone Precipitation and Solidification

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