Eosinophil peroxidase-dependent hydroxyl radical generation by human eosinophils.

McCormick, Michael L.; Roeder, Tedmund L.; Railsback, Michelle A.; Britigan, Bradley E.

doi:10.1016/s0021-9258(18)46874-3

Cited by 44 publications

(6 citation statements)

References 45 publications

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“…Eosinophil can directly produce ROS, such as superoxide and hydrogen peroxide, by eosinophil peroxidase. 22 Infiltrated eosinophils would be associated with the sustained production of 8-iso-PGE 2 at inflamed nasal mucosa in late-phase. On the other hand, mast cells produce larger amount of TXA 2 than eosinophils.…”

Section: Discussionmentioning

confidence: 99%

“…These results suggested that a certain amount of 8‐ iso ‐PGE 2 but not TXA 2 has kept in nasal mucosa. Eosinophil can directly produce ROS, such as superoxide and hydrogen peroxide, by eosinophil peroxidase 22 . Infiltrated eosinophils would be associated with the sustained production of 8‐ iso ‐PGE 2 at inflamed nasal mucosa in late‐phase.…”

Section: Discussionmentioning

confidence: 99%

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8‐ iso ‐prostaglandin E ₂ induces nasal obstruction via thromboxane receptor in murine model of allergic rhinitis

2021

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Thromboxane receptor (TP) mediates nasal obstruction, a typical symptom of allergic rhinitis. Since it has been reported that several types of eicosanoids, such as non-enzymatic oxidation product of arachidonic acid isoprostane, act as a TP ligand, there is a possibility that some other eicosanoids contribute to the TPmediated nasal obstruction. The aim of this study is to investigate the mechanisms of TP-mediated nasal obstruction. Intranasal challenges of ovalbumin (OVA) induced nasal obstruction in mice. Pharmacological blockade of TP receptor but not thromboxane A 2 synthase inhibited OVA-induced nasal obstruction. Simultaneous analysis of eicosanoids in nasal lavage fluid and the responses in trans-endothelial resistance suggested that 8-iso-prostaglandin E 2 (PGE 2 ) can be a candidate for TP ligand. Intranasal challenge of 8-iso-PGE 2 induced vascular hyperpermeability and nasal obstruction in TP receptor-dependent manner.Wholemount immunostaining of nasal septum mucosa revealed that 8-iso-PGE 2 increased plasma leakage accompanied by distention of venous sinusoids. This study shows that 8-iso-PGE 2 is a contributor in TP-mediated nasal obstruction in mice.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

8‐ iso ‐prostaglandin E ₂ induces nasal obstruction via thromboxane receptor in murine model of allergic rhinitis

2021

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“…Indeed, the use of neutralizing antibodies to TGF-β has shown to prevent organ fibrosis in murine models of different diseases ( McCormick et al, 1994 , 1999 ; Ziyadeh et al, 2000 ; Fukasawa et al, 2004 ) and in vitro ( McMillan et al, 2005 ). However, in different murine models of allergic airways disease, treatment with anti–TGF-b led to contrasting results ( McMillan et al, 2005 ; Fattouh et al, 2008 ).…”

Section: Focus On Type 2 Inflammation: the Protagonistsmentioning

confidence: 99%

Type 2 Inflammation in Eosinophilic Esophagitis: From Pathophysiology to Therapeutic Targets

et al. 2022

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Eosinophilic esophagitis (EoE) is a chronic immune-mediated disease of the esophagus characterized clinically by symptoms related to esophageal dysfunction and histologically by eosinophil-predominant inflammation, whose incidence is rising. It significantly affects patients’ quality of life and, if left untreated, results in fibrotic complications. Although broad consensus has been achieved on first-line therapy, a subset of patients remains non-responder to standard therapy. The pathogenesis of EoE is multifactorial and results from the complex, still mostly undefined, interaction between genetics and intrinsic factors, environment, and antigenic stimuli. A deep understanding of the pathophysiology of this disease is pivotal for the development of new therapies. This review provides a comprehensive description of the pathophysiology of EoE, starting from major pathogenic mechanisms (genetics, type 2 inflammation, epithelial barrier dysfunction, gastroesophageal reflux, allergens, infections and microbiota) and subsequently focusing on the single protagonists of type 2 inflammation (involved cells, cytokines, soluble effectors, surface proteins and transcription factors) that could represent present and future therapeutic targets, while summarizing previous therapeutic approaches in literature.

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“…Reactive oxidant species generated by leukocytes are of central importance in immune surveillance and host defense mechanisms; however, the reactive intermediates formed also have potential to harm normal tissue and contribute to inflammatory injury ( − ). One pathway for oxidative damage may involve formation of reactive halogenating species by the leukocyte-derived proteins, eosinophil peroxidase (EPO) and myeloperoxidase (MPO) ( − ).…”

mentioning

confidence: 99%

3-Bromotyrosine and 3,5-Dibromotyrosine Are Major Products of Protein Oxidation by Eosinophil Peroxidase: Potential Markers for Eosinophil-Dependent Tissue Injury in Vivo

et al. 1999

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Detection of specific reaction products is a powerful approach for dissecting out pathways that mediate oxidative damage in vivo. Eosinophil peroxidase (EPO), an abundant protein secreted from activated eosinophils, has been implicated in promoting oxidative tissue injury in conditions such as asthma, allergic inflammatory disorders, cancer, and helminthic infections. This unique heme protein amplifies the oxidizing potential of H2O2 by utilizing plasma levels of Br- as a cosubstrate to form potent brominating agents. Brominated products might thus serve as powerful tools for identifying sites of eosinophil-mediated tissue injury in vivo; however, structural identification and characterization of specific brominated products formed during EPO-catalyzed oxidation have not yet been reported. Here we explore the role of EPO and myeloperoxidase (MPO), a related leukocyte protein, in promoting protein oxidative damage through bromination and demonstrate that protein tyrosine residues serve as endogenous traps of reactive brominating species forming stable ring-brominated adducts. Exposure of the amino acid L-tyrosine to EPO, H2O2, and physiological concentrations of halides (100 mM Cl-,

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Eosinophil peroxidase-dependent hydroxyl radical generation by human eosinophils.

Cited by 44 publications

References 45 publications

8‐ iso ‐prostaglandin E ₂ induces nasal obstruction via thromboxane receptor in murine model of allergic rhinitis

8‐ iso ‐prostaglandin E ₂ induces nasal obstruction via thromboxane receptor in murine model of allergic rhinitis

Type 2 Inflammation in Eosinophilic Esophagitis: From Pathophysiology to Therapeutic Targets

3-Bromotyrosine and 3,5-Dibromotyrosine Are Major Products of Protein Oxidation by Eosinophil Peroxidase: Potential Markers for Eosinophil-Dependent Tissue Injury in Vivo

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Eosinophil peroxidase-dependent hydroxyl radical generation by human eosinophils.

Cited by 44 publications

References 45 publications

8‐ iso ‐prostaglandin E 2 induces nasal obstruction via thromboxane receptor in murine model of allergic rhinitis

8‐ iso ‐prostaglandin E 2 induces nasal obstruction via thromboxane receptor in murine model of allergic rhinitis

Type 2 Inflammation in Eosinophilic Esophagitis: From Pathophysiology to Therapeutic Targets

3-Bromotyrosine and 3,5-Dibromotyrosine Are Major Products of Protein Oxidation by Eosinophil Peroxidase: Potential Markers for Eosinophil-Dependent Tissue Injury in Vivo

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8‐ iso ‐prostaglandin E ₂ induces nasal obstruction via thromboxane receptor in murine model of allergic rhinitis

8‐ iso ‐prostaglandin E ₂ induces nasal obstruction via thromboxane receptor in murine model of allergic rhinitis