Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:6.3.4.6 (urease)
 7,490 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, we compared in vitro calcium binding by the taurine and glycine conjugates of the major bile acids in human bile: cholic (CA), chenodeoxycholic (CDCA) and deoxycholic (DCA) acids, together with the cholelitholytic bile acids ursodeoxycholic (UDCA) and ursocholic (UCA) acids. At physiological total calcium (CaTOT) (1-15 mM) and bile acid (BA) (10-50 mM) concentrations, all the bile acids caused concentration-dependent falls in [Ca2+], suggesting calcium binding. Except for glycine-conjugated CDCA, all the other calcium-bile acid complexes were soluble in 150 mM NaCl. The calcium binding affinities followed the pattern: dihydroxy (CDCA, UDCA and DCA) greater than trihydroxy (CA and UCA) bile acids, and glycine conjugates greater than taurine conjugates. The glycine conjugate of UDCA, which increases during UDCA treatment, had the highest calcium binding affinity. Ten-20 mM phospholipid modestly increased calcium binding by CA conjugates, but not by CDCA, UDCA, and DCA conjugates. Phospholipid also prevented the precipitation of glyco-CDCA in the presence of calcium. Bile acid-calcium biding was pH-independent over the range 6.5-8.5. The different calcium binding affinities of the major biliary bile acids may partly explain their varying effects on biliary calcium secretion. The results also suggest that neither precipitation of calcium-bile acid complexes nor impaired calcium binding by bile acids is important in the pathogenesis of human calcium gallstone formation.
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PMID:Calcium binding by bile acids: in vitro studies using a calcium ion electrode. 216 21

A microorganism with close immunohistological and genetic resemblance to Helicobacter pylori was found in the resected gallbladder mucosa of a 41-year-old woman. The woman was admitted to hospital complaining of fever and right hypochondrial pain. Cholecystectomy was carried out under the diagnosis of gallstones and cholecystitis. A microorganism resembling H. pylori (stained with H&E, Giemsa, and Wartin-Starry) was detected incidentally on pathological examination. The microorganism was also positive for immunohistochemical staining. An amplification reaction was seen on genetic examination by the polymerase chain reaction (PCR) method (urease beta-genes). Our findings suggest that H. pylori may be present in tissues other than gastric mucosa.
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PMID:Bacteria closely resembling Helicobacter pylori detected immunohistologically and genetically in resected gallbladder mucosa. 868 May 55

Recently, several authors have reported that Helicobacter pylori DNA has been found in human bile. The aim of this study is to investigate the presence of H. pylori in the biliary tree of Koreans, including the bile, biliary epithelium, and gallstones. This study analyzed intrahepatic bile, bile duct tissue, and gallstones from 43 patients with hepatobiliary disease (PTCS group), gallbladder bile and tissue from 23 patients with gallbladder disease (CCT group), and eight patients without hepatobiliary disease (control group). H. pylori was examined by PCR with two different primers. PCR was positive in 4/43 (9.3%) by 26 kDa protein antigen primer and in 5/43 (11.6%) by urease A gene primer in bile from the PTCS group. However, in intrahepatic duct tissue, PCR was positive in only one case. PCR of gallbladder bile, tissue, and intrahepatic duct stones was negative. Upon intrahepatic bile analysis, the pH was significantly lower in PCR-positive than in negative cases (P < 0.05). In conclusion, H. pylori DNA may be present in the bile when there are certain environmental changes, such as lowered pH; however, H. pylori does not colonize the bile duct epithelium. We could find no pathogenetic role for H. pylori in the formation of hepatolithiasis.
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PMID:Detection of Helicobacter pylori DNA in human biliary tree and its association with hepatolithiasis. 1096 22

In order to identify Helicobacter in gallstones of Iranian patients with biliary disease, gallstone and bile samples from 33 patients were subjected to rapid urease test, culture and Multiplex PCR using primers based on 16s rRNA and isocitrate dehydrogenase genes for the identification of Helicobacter genus and H. pylori respectively. This PCR was also done on bile samples from 40 autopsied gallbladders with normal pathology (control group). In 18.1% of stone and 12.1% of bile samples, H. pylori DNA was detected using PCR. Rapid urease and culture tests were negative for all samples. The PCR was negative in the control group. In conclusion, H. pylori DNA was detected in stone samples of Iranian patients with gallstones but we are not sure of their viability. To clarify the clinical role of Helicobacter in gallbladder diseases, studies using accurate tests on larger patient and control groups are needed to ascertain whether this microorganism is an innocent bystander or active participant in gallstone formation.
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PMID:Identification of Helicobacter pylori DNA in Iranian patients with gallstones. 1563 79

Earlier reports on the detection of Helicobacter DNA in the gallbladder tissue of patients with biliary diseases have shown discordant results. This study aimed to detect the presence of Helicobacter in gallstone, gallbladder tissue and bile specimens from subjects with H. pylori-positive gastritis with cholelithiasis. The presence of H. pylori in antrum biopsies was confirmed by rapid urease test and/or histopathological examination. DNA was extracted from gallbladder, bile and gallstone samples from 50 patients undergoing cholecystectomy. The presence of Helicobacter genus-specific DNA (16S rRNA genes) was determined by nested polymerase chain reaction assay. Helicobacter DNA was detected in the gallbladder tissue and bile of 28% and 18% respectively of the patients, but was not detected in any of the gallstones. These results do not rule out the possibility of Helicobacter infection as a contributing agent or cofactor in the development of biliary diseases.
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PMID:Presence of Helicobacter spp. DNA in the gallbladder of Egyptian patients with gallstone diseases. 2235 45

Background. The association of gallstones with Helicobacter pylori has been investigated but not clearly demonstrated. In this study, the presence of H. pylori in the gallbladder mucosa of patients with symptomatic gallstones was investigated. Method. Ninety-four consecutive patients with symptomatic gallstone disease were enrolled for the study. Gastroscopy and gastric H. pylori urease test were done before cholecystectomy to all patients who accepted. After cholecystectomy, the gallbladder tissue was investigated in terms of H. pylori by urease test, Giemsa, and immunohistochemical stain. Results. Overall 35 patients (37%) gallbladder mucosa tested positive for H. pylori with any of the three tests. Correlation of the three tests Giemsa, IHC, and rapid urease test was significant (r s : 0590, P > 0.001). Rapid urease test was positive in the gastric mucosa in 47 (58.7%) patients, and it was positive in the gallbladder mucosa in 21 patients (22%). In 15 patients both gastric and gallbladder tested positive with the urease test. There was significant correlation of rapid urease test in both of gallbladder and gastric mucosa (P = 0.0001). Conclusion. Study demonstrates the presence of H. pylori in the gallbladders of 37% of patients with symptomatic gallstones.
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PMID:Gallstones and Concomitant Gastric Helicobacter pylori Infection. 2376 37

Helicobacter hepaticus was discovered in 1992 as a cause of liver cancer in the A/JCr mouse model. In susceptible mice, infection by H. hepaticus causes chronic gastrointestinal inflammation leading to neoplasia. It can also cause morphological changes in breast-glands leading to neoplasm and adenocarcinoma in mouse models. Studies performed on humans have revealed that H. hepaticus may also be a human pathogen since infection by H. hepaticus can be associated with cholecystitis, cholelithiasis and gallbladder cancer. H. hepaticus is a close relative of H. pylori, but it lacks the major virulence factors of H. pylori including vacoulating cytotoxin A (VacA) and cytotoxin associated gene (cagA). Moreover, SabA, AlpA, and BabA, three important adhesin proteins of H. pylori, are absent in its genome. In contrast, the genome of H. hepaticus contains genes encoding some orthologus virulence factors of Campylobacter jejuni such as cytolethal distending toxin (CDT), and PebI adhesin factor. Other genes including 16S rRNA, 18 KDa immunogenic protein, and urease structural subunits are related to H. pylori. Its genome contains a small island consisting of 71 Kbp named HHGI1, which probably encodes a secretion system type IV (T4SS), and some other virulence factors. As far as the immunogenic antigens are concerned, the lipopolysaccharide (LPS) and flagellin of H. hepaticus are weak stimulants of the immune system, while pro-inflammatory responses are mainly induced by its lipoproteins and most likely by the peptidoglycan. Concerning the multidrug efflux pumps, a homologue of H. pylori TolC, HefA, has been observed in H. hepaticus which contributes to resistance to amoxicillin and bile acids.
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PMID:Helicobacter hepaticus, a new pathogenic species of the Helicobacter genus: Similarities and differences with H. pylori. 2447 22

Reports of Helicobacter pylori in biliary tract diseases in humans are very fragmentary, and therefore there is a need for further investigations. This study aims to detect H. pylori in the bile and gall bladder (GB) of patients with chronic calcular cholecystitis (CCC), and to determine the association of H. pylori infection with gallstone type. Thirty patients with CCC admitted for laparoscopic cholecystectomy were investigated, including upper gastro-endoscopy before cholecystectomy. Rapid urease test and histopathological examination were performed on gastric biopsies. The GB specimens were investigated for the presence of H. pylori by immunohistochemistry (IHC). H. pylori antigen in bile was detected by enzyme immunoassay. Chemical analysis of gallstones was performed to determine type. Immunohistochemistry testing showed 73.3% and 66.7% positivity among GB neck and body biopsies, respectively, demonstrating high sensitivity and specificity. A significant association was found between gastric and GB H. pylori positivity (P < 0.01). H. pylori antigen was detected in bile from three CCC cases. The greatest number of stones were of the calcium bilirubinate type. Gall bladder positivity for H. pylori was accompanied by chronic quiescent gastritis (40.9%). In conclusion, H. pylori infection may be an aetiological factor leading to cholecystitis. Gastric colonisation with H. pylori could be a source for GB infection, and the organism may act as a lithogenic component, especially in the context of pure pigmented gallstones.
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PMID:Detection of Helicobacter pylori infection in Egyptian patients with chronic calcular cholecystitis. 2556 97