Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.4 (trypsin)
 42,187 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Staphylococcus aureus is known to produce three very active extracellular proteinases. One of these enzymes, a cysteine proteinase, after purification to homogeneity was found to degrade insoluble bovine lung elastin at a rate comparable to human neutrophil elastase. This enzyme had no detectable activity against a range of synthetic substrates normally utilized by elastase, chymotrypsin, or trypsin-like proteinases. However, it did hydrolyze the synthetic substrate carbobenzoxy-phenylalanyl-leucyl-glutamyl-p-nitroanilide (Km = 0.5 mM, kcat = 0.16 s-1). The proteolytic activity of the cysteine proteinase was rapidly and efficiently inhibited by alpha 2-macroglobulin and also by the cysteine-specific inhibitor rat T-kininogen (Ki = 5.2 X 10(-7) M). Human kininogens, however, did not inhibit. Human plasma apparently contains other inhibitors of this enzyme, since plasma depleted of alpha 2-macroglobulin retained significant inhibitory capacity. The elastolytic activity of this S. aureus proteinase and its lack of control by human kininogens or cystatin C may explain some of the connective tissue destruction seen in bacterial infections due to this and related organisms such as may occur in septicemia, septic arthritis, and otitis.
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PMID:Degradation of elastin by a cysteine proteinase from Staphylococcus aureus. 342 37

Erythrocyte sedimentation rate is normal in 20% to 25% of patients with discitis due to common pathogens. We evaluated serum amyloid A (SAA) protein and urinary trypsin inhibitory activity in osteoarticular infections comparatively with erythrocyte sedimentation rate and serum C-reactive protein in 20 patients including 14 with discitis due to common pathogens and 6 with septic arthritis. Assays were performed on D0, D8, D15, D30, and D60 after initiation of antimicrobial therapy. On D0, all four markers were significantly higher in patients with septic arthritis than in patients with discitis. C-reactive protein levels exhibited the fastest kinetics with a return to normal values within 15 days in both conditions. Urinary trypsin inhibitory activity was only slightly elevated in patients with discitis and returned to normal within 30 days in both conditions. Serum amyloid A levels required 30 to 60 days to return to normal. Erythrocyte sedimentation rate exhibited the slowest kinetics, with normal values being achieved only after 60 days. Although simple, rapid, and inexpensive, urinary trypsin inhibitory activity determination exhibits poor sensitivity. Serum amyloid A assay is not routinely available but may be a valuable parameter for monitoring patients whose erythrocyte sedimentation rate and C-reactive protein level are normal (as in 2 of our patients with discitis).
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PMID:[Value of the assay of protein SAA and urinary antitrypsin activity in osteoarticular infections]. 805 24