Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0149520 (acute cholecystitis)
 2,784 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

57 strains of different microbial species, isolated from patients having complicated forms of acute cholecystitis, were studied with the use of the reaction of bacteriosorption on immobilized proteins: fibrinogen, fibronectin, gamma globulin, ovalbumin, etc. The reaction of bacteriosorption was positive with all 4 Staphylococcus aureus strains: they were adsorbed on fibrinogen, fibronectin and gamma globulin. Besides, 4 out of 18 Staphylococcus epidermidis strains were selectively adsorbed on fibronectin and 1 of these strains was adsorbed on ovalbumin, while 2 out of 15 Escherichia coli strains were adsorbed on ovalbumin. S. epidermidis strains studied in this work differed from 15 strains of the same species, isolated from the urine of patients and studied earlier, by their adsorption properties.
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PMID:[The binding of microorganisms isolated from patients with complicated forms of acute cholecystitis with immobilized proteins in the bacterial sorption reaction]. 207 65

Biliary complement concentrations and activity are lower in patients with infected bile than in those with sterile bile in cholecystitis. Plasma complement is increased during the acute phase response to inflammation. To determine whether low biliary complement in infected bile is a specific response to biliary tract infection or part of a general systemic reaction, we analyzed bile complement proteins (C3 and C4) and activity (C4H50) and acute phase reactants fibronectin, C-reactive protein, and alpha 1-antitrypsin concentrations in acute and chronic cholecystitis. Results were correlated with bile cultures and gallbladder histology using the Wilcoxon rank sum test. While biliary C3, C4, and C4H50 were significantly lower in infected bile than in sterile bile, none of the acute phase reactants were different. The biliary acute phase reactants were all significantly higher in acute cholecystitis than in chronic disease, but there was no difference in the biliary C3, C4, or C4H50 levels. There was no clear relationship between plasma levels of complement and the acute phase reactants. The dissociation between biliary complement and acute phase reactants indicates that bile complement is not a reflection of a systemic reaction to inflammation. We propose that biliary complement is a specific host defense mechanism against bacterial infection in the biliary tract.
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PMID:Complement in local biliary tract defense: dissociation between bile complement and acute phase reactants in cholecystitis. 349 84