Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:1.11.1.7 (peroxidase)
65,474 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Human granulocytes release 25-30% of the granular neutral proteases, collagenase and elastase, to the exterior of the cell during phagocytosis of yeast cells or immune complexes. Similar amounts of myeloperoxidase and lactoferrin are released. Crossed immunoelectrophoresis demonstrated that collagenase and elastase released extracellularly formed complexes with serum alpha1-antitrypsin. The presence of alpha1-antitrypsin complexes with granulocyte collagenase and elastase were also demonstrated in inflammatory processes, e.g. in the peritoneal exudate of acute peritonitis. The reactivity of neutrophil proteases with natural plasma protease inhibitors must be considered in assessing the role of these proteases as the etiologic agent of tissue damage and degradation during the inflammatory process.
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PMID:The extracellular release of granulocyte collagenase and elastase during phagocytosis and inflammatory processes. 19 89

Complement activation is an important step for triggering of acute inflammatory reactions. Soluble human recombinant complement receptor type 1 (sCR1) blocks complement activation by both classical and alternative pathways. In addition to glycogen-induced peritonitis, three models of complement-dependent acute inflammatory injury have been used to assess the protective effects of sCR1: lung and dermal injury after intraalveolar or intradermal deposition of IgG immune complexes; acute lung injury resulting from intravascular activation of complement after the i.v. injection of cobra venom factor; and acute skin and lung injury (at 4 h) after thermal trauma involving 25 to 30% total body surface area. Vascular injury was quantified by increases in vascular permeability, hemorrhage, neutrophil infiltration, and, as indicated, tissue water content. Intravenous infusion of sCR1 reduced lung and dermal vascular injury in all models studied. In glycogen-induced peritoneal exudates sCR1-reduced neutrophil accumulation by 79%. In animals undergoing IgG immune complex-induced alveolitis, sCR1 treatment reduced vascular permeability and hemorrhage by 72 and 71%, respectively, and tissue accumulation of neutrophils was reduced by 68%. After cobra venom factor injection, sCR1 reduced increases in lung vascular permeability by 67%, hemorrhage by 73%, and lung myeloperoxidase content by 55%. Four hours after thermal injury of skin, sCR1-treated animals demonstrated significant protection against lung injury; increases in vascular permeability and hemorrhage were reduced by 45 and 46%, respectively, and myeloperoxidase content was lowered by 39%. In thermal injury of the skin, sCR1 injection reduced dermal vascular permeability by 25% at 1 h (p = NS) and 44% at 4 h. Water content in skin biopsies was also decreased. There was a dose-response relationship between the amount of sCR1 infused and the extent of protection in each of the injury models. These data demonstrate that sCR1 offers significant protection against complement-dependent tissue injury in the animal models studied and that the protective effects are related to reduced neutrophil content.
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PMID:Protective effects of soluble CR1 in complement- and neutrophil-mediated tissue injury. 131 49

In order to study the effect of peritoneal macrophages (M phi) on conception in patients with endometriosis, the total numbers of peritoneal M phi and the proportion of the exudate type, defined on the basis of ultracytochemical localization of endogenous peroxidase (PO) activity, were investigated in 21 patients with endometriosis, five with uterine leiomyoma, three with tubal obstruction and three with carcinomatous peritonitis. An immunocytochemical observation of interleukin-1 (IL-1) was also performed in three patients with endometriosis, one with tubal obstruction, and one male patient with cholelithiasis. The total numbers of peritoneal M phi in patients with endometriosis were significantly higher than in uterine leiomyoma (2.11 x 10(7) v.s. 0.68 x 10(7), p less than 0.025). The total numbers of peritoneal M phi in tubal obstruction (0.96 x 10(7)) were not statistically different from those in uterine leiomyoma. The peritoneal M phi were remarkably increased in number in patients with carcinomatous peritonitis. On ultracytochemical observation of endogenous PO activity, the proportion of exudate M phi to whole M phi was significantly larger in endometriosis than that in uterine leiomyoma (13.3% v.s. 3.5%, p less than 0.025). This type of M phi increased even in stage I endometriosis (p less than 0.005). These data suggest that the abdominal cavity in women with endometriosis is in the stimulated conditions which may lead to infertility. A positive reaction to anti-IL-1 antibody on the cell membrane of all M phi examined in each patient suggests that an immunocytochemical study of IL-1 in M phi is not suitable for evaluating the degree of activation of M phi.
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PMID:[Activated macrophages in the peritoneal fluid of women with endometriosis: examination of the intracytoplasmic localization of endogenous peroxidase and interleukin-1]. 132 83

Peroxidase activity was assessed cytochemically in macrophages from peritoneal dialysate of 50 patients with terminal renal failure treated by intermittent peritoneal dialysis. In 22 patients cells were harvested for the second time after development of peritonitis as the complication of the treatment. The obtained results were compared with those of the control group consisting of 30 patients with normal renal function. Patients treated with peritoneal dialysis showed both in complication-free period and during the course of peritonitis significantly higher peroxidase activity in macrophages as revealed by the semiquantitative score test. In the course of peritonitis, peroxidase activity in macrophages was significantly lower than in complication-free period. Electron-microscopic cytochemistry demonstrated that in macrophages obtained from both control and dialyzed patients the peroxidase activity was located exclusively in cytoplasmic granules, suggesting a similarity of the studied cells and exudative macrophages.
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PMID:Peroxidase activity in peritoneal macrophages of patients with terminal renal failure treated by intermittent peritoneal dialysis. 215 83

Peroxidase activity was assessed cytochemically in the peritoneal dialysate neutrophils of 50 patients with terminal renal failure treated by intermittent peritoneal dialysis. In 22 patients cells were harvested for the second time after they developed peritonitis as a complication of the treatment. The results obtained were compared with those in the control group consisting of 30 patients with normal renal function. The patients treated by peritoneal dialysis showed both in the complication-free period and in the course of peritonitis significantly higher peroxidase activity in the neutrophils, as revealed by the semiquantitative score test. In the course of peritonitis, the neutrophils peroxidase activity was significantly lower than in the complication-free period.
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PMID:Peroxidase activity in peritoneal neutrophils of patients with terminal renal failure treated by intermittent peritoneal dialysis. 217 39

Impaired mental status is a poorly understood manifestation of sepsis and may be associated with altered permeability of the blood-brain barrier. To examine the possibility that sepsis affects permeability of the blood-brain barrier, rats were infected with a peritoneal implant consisting of sterilized feces, barium sulfate, and 10(8) colony forming units (CFU) of Escherichia coli. Using this model, reproducible episodes of peritonitis with bacteremia resulted. Rats were sacrificed hourly after 5 min circulation of 100 mg horseradish peroxidase. Animals were perfused-fixed and the brains removed. Representative coronal sections were stained for peroxidase reaction product and cerebral blood vessels were examined microscopically for evidence of HRP staining and extravasation. The number of stained cerebral vessels from infected rats was increased at all times compared to uninfected control rats. Extravasation of horseradish peroxide within neuropil was significantly higher in hours 1, 4 and 5 as compared to controls. The lack of significant increase in hours 2 and 3 may suggest transient closing or repair of the tight junctions. We conclude that peritonitis and bacteremia are associated with increased permeability of the blood-brain barrier.
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PMID:E. coli peritonitis and bacteremia cause increased blood-brain barrier permeability. 241 52

Despite a high concentration of serum proteins and intact phagocytes peritonitis exudates contain a large number of viable, pathogenic bacteria. The reason for this biological paradox is unknown. Our investigations reveal a pronounced defect in humoral opsonization of foreign particles in peritonitis exudate. We evaluated a modified chemiluminescence system allowing the determination of opsonic activity in serum and exudate. In serum we found a close correlation between opsonic activity and immunologically measurable levels of C3-complement and IgG. In purulent peritonitis exudates, however, the actual opsonizing activity was much less than expected according to the opsonin concentrations. We found a pronounced difference between immunologically determined opsonin levels and impaired opsonic function. Employing crossed immunoelectrophoresis massive C3-splitting into smaller fragments could be demonstrated in peritonitis exudates. In these exudates we found very high concentrations of granulocyte proteolytic (elastase) and oxidative (myeloperoxidase) enzymes which may lead to a functional destruction of opsonins followed by impaired opsonization in peritonitis exudate. The great number of bacteria and foreign particles in addition can cause a pronounced physiological consumption of complement components. The almost complete breakdown of intact C3-complement in intraabdominal exudate explains the deficient host defence in patients with severe peritonitis.
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PMID:[Insufficiency of intra-abdominal immunity to infection in purulent peritonitis--sequela of disordered foreign body opsonization]. 254 Mar 81

A deceased 59-year-old woman with insulin dependent diabetes mellitus complicated by chronic thyroiditis and chronic hepatitis was autopsied. She had had diabetes mellitus since she was 30 years old, and insulin therapy was started at 34 years. Laboratory findings were as follows: s-GOT 85, s-GPT 31, gamma-globulin 2.45 g/dl. Immunological tests were positive for anti-smooth muscle antibody and anti-ENA antibody with high titers of antithyroglobulin and anti-microsome antibodies. HLA analysis revealed the presence of DR-4. The thyroid biopsy specimen showed microscopic features characteristic of chronic thyroiditis at 52 years of age. She had been repeatedly admitted for the control of diabetes mellitus. She was admitted for the 9th time in June, 1987 following complaints of abdominal pain. After admission, her general condition became gradually worse, and she died of peritonitis in September, 1987. Pathological examination of the liver revealed an expansion of fibrous tissue on Glisson's capsule accompanied by lymphocytic infiltration and was diagnosed to be chronic inactive hepatitis. As for the thyroid gland, fibrous tissue replaced an extensive area of the thyroid gland, and normal thyroid tissue was not observed. Lymphocytic infiltration was less in comparison with that in the previous biopsy. As for the pancreas, atrophy of exocrine pancreatic tissue and fibrous change in interstitial tissue was observed. Lymphocytic infiltration was also seen in the interstitial exocrine tissue but not in the islet. Immunohistochemical examination of the islets using anti-insulin, glucagon and somatostatin antibodies by ABC peroxidase method showed the selective disappearance of B cells in the islets. The pathological changes in the thyroid gland, liver and pancreas suggest that autoimmune mechanism may be involved in the pathogenesis of chronic thyroiditis, chronic hepatitis and IDDM with exocrine pancreatic impairment in this case.
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PMID:[An autopsied case of insulin dependent diabetes mellitus complicated by chronic thyroiditis and chronic hepatitis]. 259 7

Candidal peritonitis is a tenacious infection in patients undergoing chronic peritoneal dialysis. Since little is known about host defenses of the human peritoneal cavity against fungi, we investigated the interaction of peritoneal macrophages (PM phi) from uninfected dialysis patients with Candida albicans blastospores. Chemiluminescence (CL) techniques were used to assess the respiratory burst activity of these cells, and candidacidal activity was evaluated with a fluorochrome microassay. In sharp contrast to peripheral blood polymorphonuclear leukocytes (PMNs) from healthy donors, which gave a brisk luminol-enhanced CL response to opsonized blastospores and killed 35% of cell-associated organisms, PM phi produced barely detectable luminol-enhanced CL and killed only 13% of intracellular Candida. These findings appeared to be associated with a decreased level of myeloperoxidase in PM phi. The mechanism of intracellular survival of C albicans also appeared to be related to relatively poor triggering of superoxide production during phagocytosis of viable blastospores. The CL response of PMNs to C albicans was opsonin-dependent, and peritoneal dialysis effluent was devoid of opsonic activity. These studies suggest that local cellular and humoral mechanisms of defense are inadequate for protection of peritoneal dialysis patients against candidal peritonitis.
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PMID:Intracellular survival of Candida albicans in peritoneal macrophages from chronic peritoneal dialysis patients. 300 1

In the mouse the maturation of mononuclear phagocytes was followed by comparing the ultrastructural pattern of endogenous peroxidatic activity (PA) at different time points during an acute peritonitis induced with newborn calf serum (NCS). Exudate macrophages demonstrate PA only in lysosomes, whereas resident macrophages have reaction product in the nuclear envelope (NE) and rough endoplasmic reticulum (RER). Transitional cells called "exudate-resident" macrophages have PA in the NE, RER, and some virginal lysosomes. In addition, peroxidase-negative macrophages were also present. A monoclonal antibody, F4/80, that specifically recognizes a mouse macrophage differentiation antigen (Austyn and Gordon, 1981) was used in this study. To compare the indirect immunoperoxidase labeling of this antigen and the endogenous peroxidase cytochemistry on the cellular level, a combined method was developed. Finally, the method was applied to the peritoneal cells at different time points after intraperitoneal injection of NCS in mice. The relative numbers of cells demonstrating the different patterns of endogenous PA and the proportions of each subpopulation expressing F4/80 antigen were estimated. It appeared that the expression of the antigen F4/80 coincides with the development of the resident pattern of PA. It is therefore concluded that the macrophages with the resident pattern of endogenous peroxidase are derived from monocyte-like exudate macrophages. In addition, the results indicate that both exudate-resident macrophages and at least a part of the peroxidase-negative macrophages are transitional forms.
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PMID:The development of the resident pattern of endogenous peroxidatic activity in mouse peritoneal macrophages coincides with the expression of the differentiation antigen F4/80. A combined method for immunoperoxidase labeling and endogenous peroxidase cytochemistry. 351 47


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