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)

Interleukin (IL)-1 is a pluripotential proinflammatory cytokine and is thought to be involved in the pathogenesis of bronchial asthma and late asthmatic reactions (LARs). To determine whether IL-1 plays a role in LAR, guinea pigs sensitized with Ascaris antigen were used. We evaluated IL-1 production by immunostaining with anti-IL-1 beta antibody and elucidated the action of IL-1 in LAR with recombinant IL-1 receptor antagonist. Immunostaining revealed that IL-1 beta-like immunoreactivity-positive cells increased in the airway walls and in bronchoalveolar lavage fluid after the antigen challenge. IL-1 receptor antagonist protein pretreatment reduced the generation of LAR in terms of pulmonary resistance. IL-1 receptor antagonist protein pretreatment did not change cellular components but reduced the percentage of hypodense eosinophils in bronchoalveolar lavage fluid. We also studied the direct effect of recombinant human IL-1 beta on pulmonary resistance and eosinophil activity measured as released eosinophil peroxidase activity. Recombinant human IL-1 beta did not change pulmonary resistance but primed eosinophils to release eosinophil peroxidase activity in response to platelet activating factor. Therefore these results suggest that IL-1 was produced in sensitized pulmonary tissue of guinea pigs by allergen exposure and played a role in the generation of LAR, at least partially by modulating the activation of eosinophils.
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PMID:Potential role of interleukin-1 in allergen-induced late asthmatic reactions in guinea pigs: suppressive effect of interleukin-1 receptor antagonist on late asthmatic reaction. 779 92

The mechanisms explaining the beneficial effects of glucocorticoid in ventilator-dependent preterm infants are not known. In the present randomized trial, we evaluated the hypothesis that dexamethasone (DEX) treatment of small, preterm infants at risk for chronic lung disease favorably affects the surfactant system. Twenty-three ventilator-dependent infants, with a mean +/- SD gestational age of 26 +/- 2 wk and a mean birth weight of 836 +/- 173 g, received 1 wk of treatment with either DEX (dose 0.5 mg/kg/d) or placebo beginning at 2 wk of age. The airway specimens were analyzed for surfactant components, surface activity, surfactant inhibitors, and inflammatory mediators. The concentrations of these parameters in epithelial lining fluid were calculated using the urea method. DEX treatment decreased the concentration of nonsedimentable protein in epithelial lining fluid within 3 d (p < 0.05). The nonsedimentable fraction of airway specimens decreased the surface activity of surfactant as a function of protein concentration. At a constant protein concentration, the protein from placebo-treated infants inhibited the surface activity of human surfactant in vitro more than protein from DEX-treated infants (p < 0.05). DEX transiently increased the concentration of surfactant protein-A in epithelial lining fluid but had no effect on surface activity of the sedimentable surfactant complex or on concentrations of phosphatidylcholine, IL-1 beta, lactoferrin, or myeloperoxidase. We conclude that the acute beneficial effect of DEX treatment in preterm ventilator-dependent infants may in part be mediated through a decrease in the concentration of non-sedimentable protein and a decrease in the capacity of this protein to inhibit surface activity.
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PMID:Dexamethasone treatment of infants at risk for chronic lung disease: surfactant components and inflammatory parameters in airway specimens. 780 37

The oviduct provides the environment in which fertilization of the egg and subsequent development of the preimplantation mouse embryo occurs, but little is known about the oviduct's capacity to produce growth factors or cytokines that may influence these preimplantation events. Northern blot analysis and/or immunohistochemistry were employed to examine the expression or cellular distribution, respectively, of the growth factors heparin-binding epidermal-like growth factor (HB-EGF), transforming growth factor (TGF) alpha, epidermal growth factor (EGF), insulin-like growth factor-I (IGF-I), TGF beta 1, TGF beta 2, and TGF beta 3; of estrogen-regulated lactoferrin (LF); and of the cytokines interleukin (IL)-1 alpha and IL-1 beta in the mouse oviduct during the preimplantation period (Days 1-4 [Day 1 = vaginal plug]) and 7 days after ovariectomy. The results demonstrated that, except for EGF, each of the growth factors and the LF genes are expressed in the ampulla and isthmus regions of the oviduct throughout the preimplantation period. Prominent immunostaining in secretory epithelial cells was noted for HB-EGF, TGF alpha, IGF-I, TGF beta 1, and TGF beta 2, and LF. Less intense immunostaining in the serosa and/or smooth muscle was also noted for TGF alpha, IGF-I, and TGF beta 1. In contrast, intense immunostaining in smooth muscle was noted for TGF beta 2, and TGF beta 3 was detected exclusively in smooth muscle cells. The abundance of these mRNAs was relatively constant during the preimplantation period, and ovariectomy did not reduce the levels of these mRNAs. In contrast to these growth factors, the cytokine mRNAs examined (IL-1 alpha and IL-1 beta) were at or below the limits of detection under these experimental conditions, and inflammatory leukocytes (LF-immunopositive neutrophils, IL-1 beta-immunopositive monocytes/macrophages, or peroxidase-positive eosinophils) were not detected in the oviduct, but were abundant in the adjacent uterine stroma on Day 1. These studies show that several growth factors are synthesized by the mouse oviduct and suggest that ovarian steroids do not play a major role in modulating expression of these genes in the oviduct during the preimplantation period. Furthermore, unlike the uterus on Day 1, the oviduct does not exhibit an inflammatory response to mating.
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PMID:Analysis of the expression of growth factor, interleukin-1, and lactoferrin genes and the distribution of inflammatory leukocytes in the preimplantation mouse oviduct. 781 39

The efficacy of treatment with interleukin-1 beta (IL-1 beta) and tumor necrosis factor-alpha (TNF alpha) on Pseudomonas aeruginosa pneumonia was evaluated in a granulocytopenic mouse model. Combined intravenous administration of 2000 U IL-1 beta plus 2000 U TNF alpha significantly diminished mortality from aerosol challenge with P. aeruginosa. Mice treated with IL-1 beta, TNF alpha, or both also exhibited a significant enhancement in pulmonary clearance of P. aeruginosa. Combined cytokine administration induced an increase in the pulmonary content of myeloperoxidase activity. Mature leukocytes were not detected in either circulation or bronchoalveolar lavage fluid from granulocytopenic, cytokine-treated mice. In conclusion, IL-1 beta and TNF alpha treatment exhibited a synergistic protective effect from pulmonary P. aeruginosa challenge in granulocytopenic hosts, probably due to enhancement of nonspecific antibacterial mechanisms.
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PMID:The effect of treatment with interleukin-1 and tumor necrosis factor on Pseudomonas aeruginosa lung infection in a granulocytopenic mouse model. 792 33

A new monocytic leukemia cell line (KP-1) was established from a 2-y-old Japanese girl with acute monocytic leukemia. The KP-1 cells were maintained in suspension culture with a doubling time of 96 h. The cells were positively stained with alpha-naphtyl butyrate esterase, but not with naphthol AS-D chloroacetate esterase, myeloperoxidase, and periodic acid-Schiff reagent. Cell surface marker analysis revealed that the cells were CD4, CD11a, CD11c, CD13, CD14, CD18, CD33, and HLA-DR positive. Karyotype analysis revealed near diploidy (47 XX) and a translocation t(11;19) was found. When treated with 12-o-tetradecanoylphorbol 13-acetate, KP-1 cells became tightly adherent, showed the enhanced reactivity for alpha-naphtyl butyrate esterase, and produced several monokines such as IL-1 beta, tumor necrosis factor-alpha, and macrophage colony-stimulating factor. Immunoelectron microscopy demonstrated that the human macrophage scavenger receptor was expressed after 12-o-tetradecanoylphorbol-13-acetate treatment, and the cells accumulated a large amount of cholesterol esters in the presence of acetylated LDL. Compared with another human monocytic leukemia cell line, THP-1, KP-1 expressed scavenger receptor and accumulated cholesterol ester more rapidly in the presence of 12-o-tetradecanoyl phorbol-13-acetate and acetylated LDL. Scatchard analysis using 125I-labeled acetylated LDL revealed a typical saturation curve with an apparent kd of 1.7 x 10(-7) M and 3400 binding sites per cell. KP-1 retained the characteristics of monocyte-macrophage lineage cells and will facilitate the in vitro studies of the pathologic and physiologic roles of scavenger receptors.
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PMID:Establishment and characterization of a novel human monocytic leukemia cell line (KP-1) expressing scavenger receptor. 813 64

The cytochemical characteristics and the production of tumor necrosis factor-alpha (TNF-alpha), interleukin-1 beta (IL-1 beta), and prostaglandin E2 (PGE2) by peritoneal macrophages were compared with those of blood monocytes and alveolar macrophages. The comparative percentages of mononuclear phagocytes positive for peroxidase were as follows: blood monocytes > peritoneal macrophages > alveolar macrophages. The comparative percentages of cells positive for nonspecific esterase were as follows: alveolar macrophages > peritoneal macrophages = blood monocytes. The intensity of staining for nonspecific esterase was highest in alveolar macrophages and lowest in blood monocytes. Constitutive release of TNF, IL-1 beta, and PGE2 was minimal by each cell type. Lipopolysaccharide-stimulated TNF production by alveolar macrophages was approximately five times greater than that of monocytes and 10 times greater than that of peritoneal macrophages. By contrast, lipopolysaccharide-stimulated blood monocytes produced significantly more IL-1 beta than did peritoneal or alveolar macrophages. Lipopolysaccharide-stimulated production of PGE2 by peritoneal macrophages was significantly less than that of alveolar macrophages or blood monocytes. Thus peritoneal macrophages release relatively low levels of IL-1 beta, TNF, and PGE2 in response to lipopolysaccharide. Peritoneal and alveolar macrophages differ with respect to both cytochemical characteristics and lipopolysaccharide-stimulated production of TNF and PGE2 but are similar in their limited capacity to produce IL-1 beta.
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PMID:Disparate cytochemical characteristics and production of cytokines and prostaglandin E2 by human mononuclear phagocytes from the blood, lung, and peritoneal cavity. 814 6

Previous studies in the human suggest that the interleukin-1 (IL-1) system, may be an important paracrine/autocrine mediator in local intercellular interaction in endometrial tissue. In this study we have determined that IL-1 receptor type I (IL-1R tI) is expressed at the messenger RNA (mRNA) and protein levels in glandular cells and its ligand, IL-1 beta has been localized by immunohistochemical methods in endothelial cells and isolated stromal cells in the human endometrium throughout the menstrual cycle. IL-1R tI mRNA was detected in glandular epithelium using both specific complementary DNA and complementary RNA 32P-labeled probes. Human glandular epithelium contains a 5.1-kilobase mRNA transcript throughout the complete menstrual cycle. Quantitative densitometric analysis of slot blot hybridization signals shows an increase of IL-1R tI mRNA in both early and mid-late secretory phases in comparison with the proliferative phase (P < 0.05). IL-1R tI protein was localized in endometrial glandular epithelial cells using both indirect immunofluorescence and avidin-biotin-peroxidase methods. However, more intense staining for IL-1R tI was observed in lumenal epithelial cells compared with the staining present deep in the endometrial glands. Using the same methods, IL-1 beta was detected in endothelial cells of spiral vessels and isolated stromal cells throughout the menstrual cycle, and an increased staining from proliferative to secretory phase was observed. The detection of IL-1R tI in the human endometrial epithelium and its ligand, IL-1 beta, in isolated stromal cells and endothelial cells, is another example of possible communication between the immune and reproductive systems with special relevance to human implantation.
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PMID:Localization of interleukin-1 type I receptor and interleukin-1 beta in human endometrium throughout the menstrual cycle. 834 61

Recombinant human interleukin-1 alpha, interleukin-1 beta (10, 80 or 200 units), interleukin-8 (10 or 40 units) or endotoxin was injected intravitreally into rabbit eyes. Twenty-four hours thereafter aqueous humor protein, leukocyte number, prostaglandin E2, leukotriene B4 and rabbit interleukin-1 beta were measured. In addition, synthesis of prostaglandin E2 and leukotriene B4 in iris-ciliary body and myeloperoxidase (MPO) activity were determined. Recombinant human interleukins 1 alpha and 1 beta, but not interleukin-8 induced signs of uveitis, i.e. protein and leukocytic infiltration into aqueous humor. At 200 unit activities, human interleukin-1 beta was significantly greater than interleukin-1 alpha in causing leukocyte infiltration response. Interleukin-1 alpha did not stimulate the release of prostaglandin E2 or leukotriene B4. In fact, interleukin-1 beta significantly inhibited the synthesis of prostaglandin E2 in iris-ciliary body. Both of these human interleukins caused a release of rabbit interleukin-1 beta in aqueous achieving a level significantly higher than observed after endotoxin injection. This study demonstrates that intravitreal injections of human IL-1 alpha and IL-1 beta induce uveitis by releasing rabbit interleukin-1 beta within the eye.
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PMID:Studies on intraocular inflammation produced by intravitreal human interleukins in rabbits. 838 1

To elucidate the mechanism of enhancing survival in peritonitis rats treated with lentinan, a fully purified beta-1,3-glucan, we measured the active oxygen-producing ability of polymorphonuclear leukocytes (PMNs). Four groups of rats (group I, fecal peritonitis control; II, rats receiving 3 mg/kg lentinan intraperitoneally at the same time as peritonitis induction; III, rats receiving 1 mg/kg gentamicin intramuscularly; and IV, rats receiving combined lentinan-gentamicin treatment) were used. The survival period was significantly longer in group IV than in the other three groups. The ability of ascitic PMNs to produce active oxygen (superoxide, H2O2, myeloperoxidase) was significantly more than that of blood PMNs in each group at 20 h after peritonitis induction. The increase in active oxygen production in ascitic PMNs was higher in group IV compared with that in the other three groups. The concentration of lentinan in the blood was high at 24 h after administering lentinan intraperitoneally to both the normal and peritonitis rats. In the in vitro study, the superoxide production in normal rat blood PMNs was significantly higher in the presence of cytokines (IL-1 beta, IL-6, TNF-alpha) without dose-dependence but was not higher for the lentinan group than in the control. This study therefore suggests that lentinan activated the peritoneal macrophage secretory activity and produced cytokines which thus enhanced the ability of PMNs to produce active oxygen, which possesses a bactericidal ability in PMNs.
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PMID:The ability of polymorphonuclear leukocytes to produce active oxygen in a model of peritonitis in rats. 839 70

There is evidence suggesting the importance of the interleukin-1 receptor type I (IL-1Rtl) and interleukin-1 beta (IL-1 beta) as mediator in local intercellular interactions in endometrial tissue and embryonic implantation. To complete our understanding of the entire endometrial IL-1 system in humans, we have investigated the immunohistochemical distribution of IL-1 receptor antagonist (IL-1ra) in the human endometrium throughout the menstrual cycle. We have also identified the forms of IL-1ra present in human endometrial cells. Immunoreactive IL-1ra was found in both cryostat and paraffin-embedded sections of human endometrium using the alkaline phosphatase-peroxidase (A-P) method with two different IL-1ra antibodies. IL-1ra was present throughout the entire menstrual cycle, located primarily in the endometrial epithelium. However, IL-1ra staining was significantly higher during follicular phase in comparison with early and mid-late luteal phases. Reverse transcriptase polymerase chain reaction of cultured stromal and glandular cells showed that these cells express the intracellular form of IL-1ra mRNA (icIL-1ra). Our results demonstrate the regulated presence of the icIL-1ra in the human endometrium. This finding supports a possible autocrine-paracrine role for the IL-1 system in the human endometrium and embryonic implantation.
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PMID:Immunohistochemical localization, identification and regulation of the interleukin-1 receptor antagonist in the human endometrium. 853 Jun 93


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