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proteinase inhibitor/entzündung
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Alpha-1-proteinase inhibitor in inflammatory states of humans and laboratory animals.
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Alpha-1-proteinase inhibitor (A1PI) was examined in various inflammatory conditions in terms of its capacity to inhibit leukocytic proteases and to act as a monitor of the presence of oxidants generated by stimulated leukocytes. Examination of bronchoalveolar lavage fluid from patients with
Deglycosylation of alpha 1-proteinase inhibitor is impaired in the faeces of patients with active inflammatory bowel disease (Crohn's disease).
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1. alpha 1-Proteinase inhibitor (alpha 1-antitrypsin) was excreted in the faeces of patients with inflammatory bowel disease in different molecular forms: Mr-51,000 and Mr-45,000 forms were widely found in the stools of patients with active disease, whereas a Mr-38,000 species was frequently
Urinary bikunin determination provides insight into proteinase/proteinase inhibitor imbalance in patients with inflammatory diseases.
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Bikunin (BK) is a Kunitz-type proteinase inhibitor responsible for most of the antitryptic activity of urine and so is known as the urinary trypsin inhibitor. As its excretion increases in inflammatory conditions, it is often considered to be a positive acute phase protein (APP). However, the gene
Purification of two species of exudate cysteine-proteinase inhibitors that are acute-phase reactants in the carrageenin-induced inflammation in rats.
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Two species of cysteine-proteinase inhibitors (CPIs) have been purified to homogeneity from exudate in the carrageenin-induced inflammation in rats. The exudate CPIs were separated into two forms (named CPI-1 and -2) in affinity chromatography on S-carboxymethyl-papain-Sepharose, the final stage of
Potential mediator of inflammation. Phagocyte-derived oxidants suppress the elastase-inhibitory capacity of alpha 1-proteinase inhibitor in vitro.
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Human polymorphonuclear leukocytes, monocytes, or pulmonary alveolar macrophages, stimulated in vitro by phorbol myristate acetate (PMA), released reactive oxygen species able to suppress the elastase inhibitory capacity (EIC) of human serum. Immunoelectrophoresis using antibodies against
Role of alpha 1-proteinase inhibitor in restraining peritoneal inflammation in CAPD patients.
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The concentration and functional state of alpha 1-proteinase inhibitor (alpha 1-PI) may modulate the expression of peritoneal phlogosis by affecting the activity of proteases and synthesis of autacoids. alpha 1-PI is detectable in peritoneal effluents of peritonitis-free patients. alpha 1-PI
Inactivation of alpha 1-proteinase inhibitor by alveolar inflammatory cells from smoking patients with or without emphysema.
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The aim of this study was to evaluate the ability of alveolar inflammatory cells recovered by bronchoalveolar lavage from the lower respiratory tract of 17 smoking patients with or without emphysema to inactivate alpha 1-proteinase inhibitor (alpha 1-Pl). The presence of emphysema was determined and
SERP1, a serine proteinase inhibitor encoded by myxoma virus, is a secreted glycoprotein that interferes with inflammation.
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Myxoma virus is a leporipoxvirus that causes a rapidly lethal, generalized infection known as myxomatosis in the European rabbit (Oryctolagus cuniculus). A characteristic feature of myxomatosis is the specific downregulation of key pathways important for numerous host defenses against the viral
Measurement of both native and inactivated forms of alpha1 proteinase inhibitor in human inflammatory extracellular fluids.
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BACKGROUND
Inactivation of the elastase inhibitor, alpha1 proteinase inhibitor (alpha1PI), may be of pathogenic significance in inflammatory diseases like periodontal disease. Two key mechanisms of inactivation appear to be (a) the formation of an alpha1PI-elastase complex and (b) proteolytic
Inflammatory cells degrade inter-alpha inhibitor to liberate urinary proteinase inhibitors.
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The relationship between inter-alpha inhibitor (I alpha I) and urinary proteinase inhibitor (UPI) was examined by comparing purified UPI with a proteolytic fragment of I alpha I (I'), and by demonstrating that inflammatory cells produce similar fragments under physiologic conditions. Purified I',
[Use of thermo- and acid-stable proteinase inhibitor to suppress proteolytic activation in pulmonary inflammation].
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A comparative study of thermo-acid stable proteinase inhibitor from rabbit serum and commercial drug contrykal was made on rats and in vitro experiments. Both inhibitors in equal doses effectively suppress proteolytic activity during initiation of lung inflammation. It was shown that the thermo-acid
Secretory leukoprotease inhibitor: partnering alpha 1-proteinase inhibitor to combat pulmonary inflammation.
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Secretory leukoprotease inhibitor (SLPI) is a low molecular weight serine proteinase inhibitor, notably of neutrophil elastase (NE), which is synthesised and secreted by the pulmonary epithelium. SLPI plays an important role in limiting NE-induced pulmonary inflammation and, significantly, it also
Inflammatory mediators and modulators released in organ culture from rabbit skin lesions produced in vivo by sulfur mustard. III. Electrophoretic protein fractions, trypsin-inhibitory capacity, alpha 1-proteinase inhibitor, and alpha 1- and alpha 2-macroglobulin proteinase inhibitors of culture fluids and serum.
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This is the third report in a series on the inflammatory mediators and modulators released in organ culture from skin lesions of various ages, which were produced in vivo in rabbits by the military vesicant, sulfur mustard (SM). It describes the electrophoretic protein fractions and
Vascular permeability changes by proteinase inhibitors in carrageenin-induced inflammation in rats.
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The effect of proteinase inhibitors such as TLCK, TPCK and leupeptin on vascular permeability was investigated in the carrageenin-air-pouch inflammation in rats. When each inhibitor was injected into the air-pouch immediately after carrageenin injection, TLCK, TPCK and leupeptin caused a rapid and
Proteinase inhibitors in severe inflammatory processes (septic shock and experimental endotoxaemia): biochemical, pathophysiological and therapeutic aspects.
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Plasma levels of antithrombin III, alpha 2-macroglobulin and inter-alpha-trypsin inhibitor, as well as those of various clotting, complement and other plasma factors, were significantly decreased in 18 patients suffering from hyperdynamic septic shock. A similar statistically significant reduction
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