Peroxiredoxin I is a negative regulator of Th2-dominant allergic asthma

Inoue, Ken‐ichiro; Takano, Hirohisa; Koike, Eiko; Warabi, Eiji; Yanagawa, Toru; Yanagisawa, Rie; Ishii, Tetsuro

doi:10.1016/j.intimp.2009.07.010

Cited by 25 publications

(31 citation statements)

References 45 publications

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“…The Prx6 knockout mice exhibit enhanced hypersensitivity to hyperoxia-induced lung injury (439), whereas Prx6 overexpressed mice were resistant to such damage (441). Prx1 knockout mice were also reported to be prone to bleomycin-induced lung inflammation (214) and allergic airway inflammation (187). Further, administration by N-acetyl-cysteine in Prx1 knockout mice was found to protect them against bleomycininduced acute lung injury, indicating a protective role of Prx1 against oxidative damage in inflammation (214).…”

Section: E Regulation Of Antioxidant Defense Systems In Inflammationmentioning

confidence: 99%

Reactive Oxygen Species in Inflammation and Tissue Injury

Mittal

Siddiqui

Tran

et al. 2014

Antioxidants & Redox Signaling

3,620

2,424

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Reactive oxygen species (ROS) are key signaling molecules that play an important role in the progression of inflammatory disorders. An enhanced ROS generation by polymorphonuclear neutrophils (PMNs) at the site of inflammation causes endothelial dysfunction and tissue injury. The vascular endothelium plays an important role in passage of macromolecules and inflammatory cells from the blood to tissue. Under the inflammatory conditions, oxidative stress produced by PMNs leads to the opening of inter-endothelial junctions and promotes the migration of inflammatory cells across the endothelial barrier. The migrated inflammatory cells not only help in the clearance of pathogens and foreign particles but also lead to tissue injury. The current review compiles the past and current research in the area of inflammation with particular emphasis on oxidative stress-mediated signaling mechanisms that are involved in inflammation and tissue injury. Antioxid. Redox Signal. 20, 1126-1167.

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Section: E Regulation Of Antioxidant Defense Systems In Inflammationmentioning

confidence: 99%

Reactive Oxygen Species in Inflammation and Tissue Injury

Mittal

Siddiqui

Tran

et al. 2014

Antioxidants & Redox Signaling

3,620

2,424

View full text Add to dashboard Cite

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“…PRDX1 acts as a negative regulator of Th2-dominant allergic asthma (66). Th2 differentiation, however, was not observed in Prdx1 2/2 mice during M. tuberculosis infection because cytokine/chemokine measurements showed undetectable levels of IL-4 in lungs of M. tuberculosis-infected Prdx1 2/2 mice and the same levels of IL-5, IL-9, and IL-13 in lungs of Prdx1 2/2 and WT mice during M. tuberculosis infection (Fig.…”

Section: Discussionmentioning

confidence: 99%

Peroxiredoxin 1 Contributes to Host Defenses against Mycobacterium tuberculosis

Matsumura

Iwai

Kato-Miyazawa

et al. 2016

The Journal of Immunology

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Peroxiredoxin (PRDX)1 is an antioxidant that detoxifies hydrogen peroxide and peroxinitrite. Compared with wild-type (WT) mice, Prdx1-deficient (Prdx1−/−) mice showed increased susceptibility to Mycobacterium tuberculosis and lower levels of IFN-γ and IFN-γ–producing CD4+ T cells in the lungs after M. tuberculosis infection. IL-12 production, c-Rel induction, and p38 MAPK activation levels were lower in Prdx1−/− than in WT bone marrow–derived macrophages (BMDMs). IFN-γ–activated Prdx1−/− BMDMs did not kill M. tubercuosis effectively. NO production levels were lower, and arginase activity and arginase 1 (Arg1) expression levels were higher, in IFN-γ–activated Prdx1−/− than in WT BMDMs after M. tuberculosis infection. An arginase inhibitor, Nω-hydroxy-nor-arginine, restored antimicrobial activity and NO production in IFN-γ–activated Prdx1−/− BMDMs after M. tuberculosis infection. These results suggest that PRDX1 contributes to host defenses against M. tuberculosis. PRDX1 positively regulates IL-12 production by inducing c-Rel and activating p38 MAPK, and it positively regulates NO production by suppressing Arg1 expression in macrophages infected with M. tuberculosis.

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“…Moreover, levels of superoxide dismutase (spot 19) and peroxiredoxin 1 (spot 22) were also increased in our proteomic data. Recent studies have revealed that both play a critical role in protecting the lungs against oxidative damage and are involved in the development of asthma (31,32). Actin Cytoskeleton, Integrin, and Focal Adhesion Kinase Signaling-Actin cytoskeletal signaling participates in many fundamental processes, including the regulation of cell shape, migration, and adhesion.…”

Section: Discussionmentioning

confidence: 99%

The Protease Allergen Pen c 13 Induces Allergic Airway Inflammation and Changes in Epithelial Barrier Integrity and Function in a Murine Model

Chen

Chuang

et al. 2011

Journal of Biological Chemistry

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Fungal allergens are associated with the development of asthma, and some have been characterized as proteases. Here, we established an animal model of allergic airway inflammation in response to continuous exposure to proteolytically active Pen c 13, a major allergen secreted by Penicillium citrinum. In functional analyses, Pen c 13 exposure led to increased airway hyperresponsiveness, significant inflammatory cell infiltration, mucus overproduction, and collagen deposition in the lung, dramatically elevated serum levels of total IgE and Pen c 13-specific IgE and IgG1, and increased production of the Th2 cytokines IL-4, IL-5, and IL-13 by splenocytes stimulated in vitro with Pen c 13. To examine the mechanisms involved in the regulation of allergenicity by Pen c 13, we performed two-dimensional fluorescence difference gel electrophoresis analysis combined with nano-LC-MS/MS, followed by bioinformatics analysis to identify potential targets that associated with allergic inflammation, which suggested that galectin-3 and laminin might be involved in novel pathogenic mechanisms. Finally, we focused on junctional proteins between cells, because, in addition to opening of the epithelial barrier by environmental proteases possibly being the initial step in the development of asthma, these proteins are also associated with actin rearrangement. Taken together, our findings indicate that Pen c 13 exposure causes junctional structure alterations and actin cytoskeletal rearrangements, resulting in increased permeability and airway structural changes. These effects probably change the lung microenvironment and foster the development of allergic sensitization.

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Peroxiredoxin I is a negative regulator of Th2-dominant allergic asthma

Cited by 25 publications

References 45 publications

Reactive Oxygen Species in Inflammation and Tissue Injury

Reactive Oxygen Species in Inflammation and Tissue Injury

Peroxiredoxin 1 Contributes to Host Defenses against Mycobacterium tuberculosis

The Protease Allergen Pen c 13 Induces Allergic Airway Inflammation and Changes in Epithelial Barrier Integrity and Function in a Murine Model

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