Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.2.1.31 (beta-glucuronidase)
 7,680 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Bile pigment gallstones were produced in six of six mongrel dogs by narrowing the cystic duct with ligature after a postoperative interval of seven days. beta-Glucuronidase producing group G Streptococcus and Staphylococcus aureus were found in the bile, the gallbladder wall, and the liver. In another trial similar gallstones were produced in four of eight dogs after mere injection of beta-glucuronidase producing Escherichia coli into the spleen resp. in six of eight dogs after injection of E. coli into the colon without ligature of the cystic duct. In an additional series gallstones were produced in six dogs after injection of beta-glucuronidase producing E. coli into the colon plus ligature of the cystic duct. The injected strain of E. coli was found in the bile, the gallbladder wall, the liver, and even within the produced gallstones. In a control group in none of six dogs gallstones were present. beta-Glucuronidase producing group G Streptococcus was found in the gallbladder of one dog, Pseudomonas aeruginosa was found in the gallbladder of another dog and Staphylococcus aureus in the liver and gallbladder wall of a third dog. We conclude from our experiments that merely bacterial infection of the biliary tract can lead to gallstone formation. The bacterial colonization of the liver and the biliary tract is promoted by biliary tract obstruction. beta-Glucuronidase producing bacteria increase the amount of beta-glucuronidase in the bile thus leading to calcium bilirubinate precipitation and gallstone formation by deconjugation of bilirubindiglucuronide.
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PMID:[Experimental gallstone formation. Etiological significance of beta-glucuronidase producing bacteria and biliary obstruction]. 685 81

To investigate the effects of strenuous forced exercise on the course and complications of a bacterial infection and on myocardial responses and performance capacity, rats with tularemia (characterized by pyogranulomatous hepatic and splenic lesions) were exercised by swimming on days 0-6 of infection. Levels of glutamic oxaloacetic and pyruvic transaminases in plasma, densities of pyogranulomatous lesions, and bacterial counts in blood, liver, and spleen were similar in exercising and resting rats. Although a few exercising rats showed an unusual dissemination of infection, the antibody responses were similar in rest and exercise. Plasma concentrations of beta-glucuronidase, lysozyme and alpha 2-macrofetoprotein were higher with exercise, a result that indicated that more vigorous stress responses were elicited with exercise than with infection alone. Physical performance capacity was reduced by the infection, but forced daily exercise limited this reduction substantially and counteracted the myocardial protein-degrading effects of infection. Thus, exercise evoked normal training responses even during this generalized infection.
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PMID:The effects of strenuous exercise on infection with Francisella tularensis in rats. 707 93

Pseudomonas aeruginosa infection frequently complicates lung injury and can be fatal in immunocompromised or debilitated individuals. Previous studies from our laboratory indicate that elastase from P. aeruginosa increases epithelial permeability by disrupting tight junctions between epithelial cells. Because the inflammatory reaction of the host is a prominent feature of bacterial infection, we reasoned that additional virulence factors from this organism could extend and augment the initial pulmonary injury by prompting accumulation of neutrophils. To test this hypothesis, we compared responses of guinea pigs to aerosols of elastase (PE) and lipopolysaccharide (LPS) from P. aeruginosa. After each treatment, we measured epithelial permeability and accumulation of neutrophils, interleukin 8 (IL-8), and beta-glucuronidase in epithelial lining fluid (ELF). We found that PE increased epithelial permeability, as measured by both the clearance of aerosolized radiolabeled albumin from the air spaces and the concentration of plasma albumin in epithelial lining fluid, but it was less effective than LPS at recruiting neutrophils into the lungs. In contrast, LPS had no significant effect on epithelium, but it increased the concentration of neutrophils, IL-8, and beta-glucuronidase in ELF. Increased epithelial permeability induced by PE does not cause lung inflammation, but it may facilitate the LPS-induced influx of neutrophils.
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PMID:Virulence factors from Pseudomonas aeruginosa increase lung epithelial permeability. 1114 11

The activation of the CAChi2 promoter as the result of bacterial infection and osmotic stresses was examined using the Agrobacterium-mediated transient expression assay. Several stress-related cis-acting elements were revealed within the upstream genomic sequence of the CAChi2 gene. In tobacco leaf tissues transiently transformed with the CAChi2 promoter-beta-glucuronidase (GUS) gene, the CAChi2 promoter was up-regulated by Pseudomonas syringae pv. tabaci infection. The CAChi2-GUS activation was closely related to osmotic stresses, including treatment with mannitol and NaCl. The -378 CAChi2 promoter was sufficient for the CAChi2 gene induction by salicylic acid treatment. CAChi2 overexpression in the transgenic Arabidopsis plants enhanced bacterial disease resistance against Pseudomonas syringae pv. tomato infection. CAChi2-overexpressing Arabidopsis plants also exhibited increased tolerance to NaCl-induced osmotic stresses during seed germination and seedling growth. CAChi2 overexpression induced the expression of the NaCl stress-responsive gene RD29A in the absence of NaCl stress. The CAChi2-overexpressing transgenic plants exhibited increased sensitivity to abscisic acid during seed germination.
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PMID:Promoter activation of pepper class II basic chitinase gene, CAChi2, and enhanced bacterial disease resistance and osmotic stress tolerance in the CAChi2-overexpressing Arabidopsis. 1615 43

The MtEnod11 gene from Medicago truncatula is widely used as an early infection-related molecular marker for endosymbiotic associations involving both rhizobia and arbuscular mycorrhizal fungi. In this article, heterologous expression of the MtEnod11 promoter has been studied in two actinorhizal trees, Casuarina glauca and Allocasuarina verticillata. Transgenic C. glauca and A. verticillata expressing a ProMtEnod11::beta-glucuronidase (gus) fusion were generated and the activation of the transgene investigated in the context of the symbiotic associations with the N-fixing actinomycete Frankia and both endo- and ectomycorrhizal fungi (Glomus intraradices and Pisolithus albus, respectively). ProMtEnod11::gus expression was observed in root hairs, prenodules, and nodules and could be correlated with the infection of plant cells by Frankia spp. However, no activation of the gus reporter gene was detected prior to infection or in response to either rhizobial Nod factors or the wasp venom peptide MAS-7. Equally, ProMtEnod11::gus expression was not elicited during the symbiotic associations with either ecto- or endomycorrhizal fungi. These observations suggest that, although there is a conservation of gene regulatory pathways between legumes and actinorhizal plants in cells accommodating endosymbiotic N-fixing bacteria, the events preceding bacterial infection or related to mycorrhization appear to be less conserved.
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PMID:Infection-specific activation of the Medicago truncatula Enod11 early nodulin gene promoter during actinorhizal root nodulation. 2045 13


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