Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.2.1.36 (hyaluronidase)
 4,606 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Thirty isolates of Clostridium difficile expressing different degrees of toxigenicity and virulence in an animal model were assayed for the production of chondroitin-4-sulphatase, hyaluronidase, heparinase, collagenase and protease. All strains demonstrated some hydrolytic enzyme activity. There was no direct correlation between toxigenic status, or virulence, and hydrolytic enzyme production. However, all five strains known to be highly virulent in the hamster model had hyaluronidase, chondroitin-4-sulphatase and collagenase activity whereas only three of five toxigenic but poorly virulent strains had these activities, the collagenase activity being weak in all three cases. The only two proteolytic strains are also highly virulent. The potential tissue damaging properties of these hydrolytic enzymes may help to explain the differences in virulence of C. difficile strains seen in the Syrian hamster model of antibiotic-associated colitis, and may contribute to the spectrum of disease seen in man. It is also possible that chondroitin-4-sulphatase, hyaluronidase and collagenase activity may release essential nutrients, promoting establishment of C. difficile in the gut.
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PMID:Hydrolytic enzyme production by Clostridium difficile and its relationship to toxin production and virulence in the hamster model. 215 75

Platelets are specialized cells essential for hemostasis that also function as crucial effectors capable of mediating inflammatory and immune responses. These sentinels continually survey their environment and discriminate between homeostatic and danger signals such as modified components of the extracellular matrix. The glycosaminoglycan hyaluronan (HA) is a major extracellular matrix component that coats the vascular lumen and, under normal conditions, restricts access of inflammatory cells. In response to tissue damage, the endothelial HA matrix enhances leukocyte recruitment and regulates the early stages of the inflammatory response. We have shown that platelets can degrade HA from the surface of activated endothelial cells via the enzyme hyaluronidase-2 (HYAL2) and that HYAL2 is deficient in platelets isolated from patients with inflammatory bowel disease (IBD). Platelets are known to be involved in the pathogenesis of several chronic disease states, including IBD, but they have been largely overlooked in the context of intestinal inflammation. We therefore wanted to define the mechanism by which platelet HYAL2 regulates the inflammatory response during colitis. In this study, we provide evidence that HA catabolism is disrupted in human intestinal microvascular endothelial cells isolated from patients with IBD. Furthermore, mice deficient in HYAL2 are more susceptible to an acute model of colitis, and this increased susceptibility is abrogated by transfusion of HYAL2-competent platelets. Finally, we show that platelets, via HYAL2-dependent degradation of endothelial HA, regulate the early stages of inflammation in colitis by limiting leukocyte extravasation.
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PMID:Platelet hyaluronidase-2 regulates the early stages of inflammatory disease in colitis. 3126 81