Ablation of Glutaredoxin-1 Modulates House Dust Mite-Induced Allergic Airways Disease in Mice.
Identifieur interne : 000480 ( Main/Exploration ); précédent : 000479; suivant : 000481Ablation of Glutaredoxin-1 Modulates House Dust Mite-Induced Allergic Airways Disease in Mice.
Auteurs : Sidra M. Hoffman ; Xi Qian ; James D. Nolin ; David G. Chapman [États-Unis] ; Shi Biao Chia ; Karolyn G. Lahue ; Robert Schneider ; Jennifer L. Ather [États-Unis] ; Matthew J. Randall [États-Unis] ; David H. Mcmillan ; Jane T. Jones ; Douglas J. Taatjes ; Minara Aliyeva [États-Unis] ; Nirav Daphtary [États-Unis] ; Sarah Abdalla ; Lennart K A. Lundblad [États-Unis] ; Ye-Shih Ho ; Vikas Anathy ; Charles G. Irvin [États-Unis] ; Emiel F M. Wouters [Pays-Bas] ; Niki L. Reynaert [Pays-Bas] ; Anne E. Dixon [États-Unis] ; Albert Van Der Vliet ; Matthew E. Poynter [États-Unis] ; Yvonne M W. Janssen-HeiningerSource :
- American journal of respiratory cell and molecular biology [ 1535-4989 ] ; 2016.
Descripteurs français
- KwdFr :
- ARN messager (génétique), ARN messager (métabolisme), Animaux (MeSH), Cytokines (génétique), Cytokines (métabolisme), Glutarédoxines (métabolisme), Glutathion (métabolisme), Hyperplasie (MeSH), Hypersensibilité (anatomopathologie), Hypersensibilité (complications), Hypersensibilité (parasitologie), Hypersensibilité (sang), Hypersensibilité respiratoire (anatomopathologie), Hypersensibilité respiratoire (parasitologie), Hypersensibilité respiratoire (physiopathologie), Hypersensibilité respiratoire (sang), Immunoglobuline E (sang), Immunoglobuline G (sang), Lymphocytes auxiliaires Th2 (immunologie), Mucus (métabolisme), Mécanique respiratoire (MeSH), Pneumopathie infectieuse (anatomopathologie), Pneumopathie infectieuse (complications), Pneumopathie infectieuse (parasitologie), Pneumopathie infectieuse (sang), Poumon (anatomopathologie), Poumon (parasitologie), Pyroglyphidae (physiologie), Souris de lignée BALB C (MeSH).
- MESH :
- anatomopathologie : Hypersensibilité, Hypersensibilité respiratoire, Pneumopathie infectieuse, Poumon.
- génétique : ARN messager, Cytokines, Hypersensibilité, Pneumopathie infectieuse.
- immunologie : Lymphocytes auxiliaires Th2.
- métabolisme : ARN messager, Cytokines, Glutarédoxines, Glutathion, Mucus.
- parasitologie : Hypersensibilité, Hypersensibilité respiratoire, Pneumopathie infectieuse, Poumon.
- physiologie : Pyroglyphidae.
- physiopathologie : Hypersensibilité respiratoire.
- sang : Hypersensibilité, Hypersensibilité respiratoire, Immunoglobuline E, Immunoglobuline G, Pneumopathie infectieuse.
- Animaux, Hyperplasie, Mécanique respiratoire, Souris de lignée BALB C.
English descriptors
- KwdEn :
- Animals (MeSH), Cytokines (genetics), Cytokines (metabolism), Glutaredoxins (metabolism), Glutathione (metabolism), Hyperplasia (MeSH), Hypersensitivity (blood), Hypersensitivity (complications), Hypersensitivity (parasitology), Hypersensitivity (pathology), Immunoglobulin E (blood), Immunoglobulin G (blood), Lung (parasitology), Lung (pathology), Mice, Inbred BALB C (MeSH), Mucus (metabolism), Pneumonia (blood), Pneumonia (complications), Pneumonia (parasitology), Pneumonia (pathology), Pyroglyphidae (physiology), RNA, Messenger (genetics), RNA, Messenger (metabolism), Respiratory Hypersensitivity (blood), Respiratory Hypersensitivity (parasitology), Respiratory Hypersensitivity (pathology), Respiratory Hypersensitivity (physiopathology), Respiratory Mechanics (MeSH), Th2 Cells (immunology).
- MESH :
- chemical , blood : Immunoglobulin E, Immunoglobulin G.
- chemical , genetics : Cytokines, RNA, Messenger.
- chemical , metabolism : Cytokines, Glutaredoxins, Glutathione, RNA, Messenger.
- blood : Hypersensitivity, Pneumonia, Respiratory Hypersensitivity.
- complications : Hypersensitivity, Pneumonia.
- immunology : Th2 Cells.
- metabolism : Mucus.
- parasitology : Hypersensitivity, Lung, Pneumonia, Respiratory Hypersensitivity.
- pathology : Hypersensitivity, Lung, Pneumonia, Respiratory Hypersensitivity.
- physiology : Pyroglyphidae.
- physiopathology : Respiratory Hypersensitivity.
- Animals, Hyperplasia, Mice, Inbred BALB C, Respiratory Mechanics.
Abstract
Protein S-glutathionylation (PSSG) is an oxidant-induced post-translational modification of protein cysteines that impacts structure and function. The oxidoreductase glutaredoxin-1 (Glrx1) under physiological conditions catalyzes deglutathionylation and restores the protein thiol group. The involvement of Glrx1/PSSG in allergic inflammation induced by asthma-relevant allergens remains unknown. In the present study, we examined the impact of genetic ablation of Glrx1 in the pathogenesis of house dust mite (HDM)-induced allergic airways disease in mice. Wild-type (WT) or Glrx1(-/-) mice were instilled intranasally with HDM on 5 consecutive days for 3 weeks. As expected, overall PSSG was increased in Glrx1(-/-) HDM mice as compared with WT animals. Total cells in bronchoalveolar lavage fluid were similarly increased in HDM-treated WT and Glrx1(-/-) mice. However, in response to HDM, mice lacking Glrx1 demonstrated significantly more neutrophils and macrophages but fewer eosinophils as compared with HDM-exposed WT mice. mRNA expression of the Th2-associated cytokines IL-13 and IL-6, as well as mucin-5AC (Muc5ac), was significantly attenuated in Glrx1(-/-) HDM-treated mice. Conversely, mRNA expression of IFN-γ and IL-17A was increased in Glrx1(-/-) HDM mice compared with WT littermates. Restimulation of single-cell suspensions isolated from lungs or spleens with HDM resulted in enhanced IL-17A and decreased IL-5 production in cells derived from inflamed Glrx1(-/-) mice compared with WT animals. Finally, HDM-induced tissue damping and elastance were significantly attenuated in Glrx1(-/-) mice compared with WT littermates. These results demonstrate that the Glrx1-PSSG axis plays a pivotal role in HDM-induced allergic airways disease in association with enhanced type 2 inflammation and restriction of IFN-γ and IL-17A.
DOI: 10.1165/rcmb.2015-0401OC
PubMed: 27035878
PubMed Central: PMC5023028
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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<author><name sortKey="Poynter, Matthew E" sort="Poynter, Matthew E" uniqKey="Poynter M" first="Matthew E" last="Poynter">Matthew E. Poynter</name>
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</placeName>
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<author><name sortKey="Janssen Heininger, Yvonne M W" sort="Janssen Heininger, Yvonne M W" uniqKey="Janssen Heininger Y" first="Yvonne M W" last="Janssen-Heininger">Yvonne M W. Janssen-Heininger</name>
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<sourceDesc><biblStruct><analytic><title xml:lang="en">Ablation of Glutaredoxin-1 Modulates House Dust Mite-Induced Allergic Airways Disease in Mice.</title>
<author><name sortKey="Hoffman, Sidra M" sort="Hoffman, Sidra M" uniqKey="Hoffman S" first="Sidra M" last="Hoffman">Sidra M. Hoffman</name>
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<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Qian, Xi" sort="Qian, Xi" uniqKey="Qian X" first="Xi" last="Qian">Xi Qian</name>
<affiliation><nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Nolin, James D" sort="Nolin, James D" uniqKey="Nolin J" first="James D" last="Nolin">James D. Nolin</name>
<affiliation><nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Chapman, David G" sort="Chapman, David G" uniqKey="Chapman D" first="David G" last="Chapman">David G. Chapman</name>
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<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Chia, Shi Biao" sort="Chia, Shi Biao" uniqKey="Chia S" first="Shi Biao" last="Chia">Shi Biao Chia</name>
<affiliation><nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Lahue, Karolyn G" sort="Lahue, Karolyn G" uniqKey="Lahue K" first="Karolyn G" last="Lahue">Karolyn G. Lahue</name>
<affiliation><nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Schneider, Robert" sort="Schneider, Robert" uniqKey="Schneider R" first="Robert" last="Schneider">Robert Schneider</name>
<affiliation><nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Ather, Jennifer L" sort="Ather, Jennifer L" uniqKey="Ather J" first="Jennifer L" last="Ather">Jennifer L. Ather</name>
<affiliation wicri:level="2"><nlm:affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Randall, Matthew J" sort="Randall, Matthew J" uniqKey="Randall M" first="Matthew J" last="Randall">Matthew J. Randall</name>
<affiliation wicri:level="2"><nlm:affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Mcmillan, David H" sort="Mcmillan, David H" uniqKey="Mcmillan D" first="David H" last="Mcmillan">David H. Mcmillan</name>
<affiliation><nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Jones, Jane T" sort="Jones, Jane T" uniqKey="Jones J" first="Jane T" last="Jones">Jane T. Jones</name>
<affiliation><nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Taatjes, Douglas J" sort="Taatjes, Douglas J" uniqKey="Taatjes D" first="Douglas J" last="Taatjes">Douglas J. Taatjes</name>
<affiliation><nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Aliyeva, Minara" sort="Aliyeva, Minara" uniqKey="Aliyeva M" first="Minara" last="Aliyeva">Minara Aliyeva</name>
<affiliation wicri:level="2"><nlm:affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Daphtary, Nirav" sort="Daphtary, Nirav" uniqKey="Daphtary N" first="Nirav" last="Daphtary">Nirav Daphtary</name>
<affiliation wicri:level="2"><nlm:affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Abdalla, Sarah" sort="Abdalla, Sarah" uniqKey="Abdalla S" first="Sarah" last="Abdalla">Sarah Abdalla</name>
<affiliation><nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Lundblad, Lennart K A" sort="Lundblad, Lennart K A" uniqKey="Lundblad L" first="Lennart K A" last="Lundblad">Lennart K A. Lundblad</name>
<affiliation wicri:level="2"><nlm:affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Ho, Ye Shih" sort="Ho, Ye Shih" uniqKey="Ho Y" first="Ye-Shih" last="Ho">Ye-Shih Ho</name>
<affiliation><nlm:affiliation>3 Institute of Environmental Health Sciences, Wayne State University, Detroit, Michigan; and.</nlm:affiliation>
<wicri:noCountry code="subField">Michigan; and</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Anathy, Vikas" sort="Anathy, Vikas" uniqKey="Anathy V" first="Vikas" last="Anathy">Vikas Anathy</name>
<affiliation><nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Irvin, Charles G" sort="Irvin, Charles G" uniqKey="Irvin C" first="Charles G" last="Irvin">Charles G. Irvin</name>
<affiliation wicri:level="2"><nlm:affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Wouters, Emiel F M" sort="Wouters, Emiel F M" uniqKey="Wouters E" first="Emiel F M" last="Wouters">Emiel F M. Wouters</name>
<affiliation wicri:level="1"><nlm:affiliation>4 Department of Respiratory Medicine, Maastricht University Medical Center, Maastricht, the Netherlands.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">Pays-Bas</country>
<wicri:regionArea>4 Department of Respiratory Medicine, Maastricht University Medical Center, Maastricht</wicri:regionArea>
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</affiliation>
</author>
<author><name sortKey="Reynaert, Niki L" sort="Reynaert, Niki L" uniqKey="Reynaert N" first="Niki L" last="Reynaert">Niki L. Reynaert</name>
<affiliation wicri:level="1"><nlm:affiliation>4 Department of Respiratory Medicine, Maastricht University Medical Center, Maastricht, the Netherlands.</nlm:affiliation>
<country xml:lang="fr" wicri:curation="lc">Pays-Bas</country>
<wicri:regionArea>4 Department of Respiratory Medicine, Maastricht University Medical Center, Maastricht</wicri:regionArea>
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</affiliation>
</author>
<author><name sortKey="Dixon, Anne E" sort="Dixon, Anne E" uniqKey="Dixon A" first="Anne E" last="Dixon">Anne E. Dixon</name>
<affiliation wicri:level="2"><nlm:affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Van Der Vliet, Albert" sort="Van Der Vliet, Albert" uniqKey="Van Der Vliet A" first="Albert" last="Van Der Vliet">Albert Van Der Vliet</name>
<affiliation><nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
</author>
<author><name sortKey="Poynter, Matthew E" sort="Poynter, Matthew E" uniqKey="Poynter M" first="Matthew E" last="Poynter">Matthew E. Poynter</name>
<affiliation wicri:level="2"><nlm:affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</nlm:affiliation>
<country xml:lang="fr">États-Unis</country>
<placeName><region type="state">Vermont</region>
</placeName>
<wicri:cityArea>2 Medicine, University of Vermont, Burlington</wicri:cityArea>
</affiliation>
</author>
<author><name sortKey="Janssen Heininger, Yvonne M W" sort="Janssen Heininger, Yvonne M W" uniqKey="Janssen Heininger Y" first="Yvonne M W" last="Janssen-Heininger">Yvonne M W. Janssen-Heininger</name>
<affiliation><nlm:affiliation>Departments of 1 Pathology and Laboratory Medicine and.</nlm:affiliation>
<wicri:noCountry code="no comma">Departments of 1 Pathology and Laboratory Medicine and.</wicri:noCountry>
</affiliation>
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<series><title level="j">American journal of respiratory cell and molecular biology</title>
<idno type="eISSN">1535-4989</idno>
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<term>Cytokines (genetics)</term>
<term>Cytokines (metabolism)</term>
<term>Glutaredoxins (metabolism)</term>
<term>Glutathione (metabolism)</term>
<term>Hyperplasia (MeSH)</term>
<term>Hypersensitivity (blood)</term>
<term>Hypersensitivity (complications)</term>
<term>Hypersensitivity (parasitology)</term>
<term>Hypersensitivity (pathology)</term>
<term>Immunoglobulin E (blood)</term>
<term>Immunoglobulin G (blood)</term>
<term>Lung (parasitology)</term>
<term>Lung (pathology)</term>
<term>Mice, Inbred BALB C (MeSH)</term>
<term>Mucus (metabolism)</term>
<term>Pneumonia (blood)</term>
<term>Pneumonia (complications)</term>
<term>Pneumonia (parasitology)</term>
<term>Pneumonia (pathology)</term>
<term>Pyroglyphidae (physiology)</term>
<term>RNA, Messenger (genetics)</term>
<term>RNA, Messenger (metabolism)</term>
<term>Respiratory Hypersensitivity (blood)</term>
<term>Respiratory Hypersensitivity (parasitology)</term>
<term>Respiratory Hypersensitivity (pathology)</term>
<term>Respiratory Hypersensitivity (physiopathology)</term>
<term>Respiratory Mechanics (MeSH)</term>
<term>Th2 Cells (immunology)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr"><term>ARN messager (génétique)</term>
<term>ARN messager (métabolisme)</term>
<term>Animaux (MeSH)</term>
<term>Cytokines (génétique)</term>
<term>Cytokines (métabolisme)</term>
<term>Glutarédoxines (métabolisme)</term>
<term>Glutathion (métabolisme)</term>
<term>Hyperplasie (MeSH)</term>
<term>Hypersensibilité (anatomopathologie)</term>
<term>Hypersensibilité (complications)</term>
<term>Hypersensibilité (parasitologie)</term>
<term>Hypersensibilité (sang)</term>
<term>Hypersensibilité respiratoire (anatomopathologie)</term>
<term>Hypersensibilité respiratoire (parasitologie)</term>
<term>Hypersensibilité respiratoire (physiopathologie)</term>
<term>Hypersensibilité respiratoire (sang)</term>
<term>Immunoglobuline E (sang)</term>
<term>Immunoglobuline G (sang)</term>
<term>Lymphocytes auxiliaires Th2 (immunologie)</term>
<term>Mucus (métabolisme)</term>
<term>Mécanique respiratoire (MeSH)</term>
<term>Pneumopathie infectieuse (anatomopathologie)</term>
<term>Pneumopathie infectieuse (complications)</term>
<term>Pneumopathie infectieuse (parasitologie)</term>
<term>Pneumopathie infectieuse (sang)</term>
<term>Poumon (anatomopathologie)</term>
<term>Poumon (parasitologie)</term>
<term>Pyroglyphidae (physiologie)</term>
<term>Souris de lignée BALB C (MeSH)</term>
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<keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Immunoglobulin E</term>
<term>Immunoglobulin G</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Cytokines</term>
<term>RNA, Messenger</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Cytokines</term>
<term>Glutaredoxins</term>
<term>Glutathione</term>
<term>RNA, Messenger</term>
</keywords>
<keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Hypersensibilité</term>
<term>Hypersensibilité respiratoire</term>
<term>Pneumopathie infectieuse</term>
<term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="blood" xml:lang="en"><term>Hypersensitivity</term>
<term>Pneumonia</term>
<term>Respiratory Hypersensitivity</term>
</keywords>
<keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Hypersensitivity</term>
<term>Pneumonia</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr"><term>ARN messager</term>
<term>Cytokines</term>
<term>Hypersensibilité</term>
<term>Pneumopathie infectieuse</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Lymphocytes auxiliaires Th2</term>
</keywords>
<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Th2 Cells</term>
</keywords>
<keywords scheme="MESH" qualifier="metabolism" xml:lang="en"><term>Mucus</term>
</keywords>
<keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>ARN messager</term>
<term>Cytokines</term>
<term>Glutarédoxines</term>
<term>Glutathion</term>
<term>Mucus</term>
</keywords>
<keywords scheme="MESH" qualifier="parasitologie" xml:lang="fr"><term>Hypersensibilité</term>
<term>Hypersensibilité respiratoire</term>
<term>Pneumopathie infectieuse</term>
<term>Poumon</term>
</keywords>
<keywords scheme="MESH" qualifier="parasitology" xml:lang="en"><term>Hypersensitivity</term>
<term>Lung</term>
<term>Pneumonia</term>
<term>Respiratory Hypersensitivity</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Hypersensitivity</term>
<term>Lung</term>
<term>Pneumonia</term>
<term>Respiratory Hypersensitivity</term>
</keywords>
<keywords scheme="MESH" qualifier="physiologie" xml:lang="fr"><term>Pyroglyphidae</term>
</keywords>
<keywords scheme="MESH" qualifier="physiology" xml:lang="en"><term>Pyroglyphidae</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Hypersensibilité respiratoire</term>
</keywords>
<keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Respiratory Hypersensitivity</term>
</keywords>
<keywords scheme="MESH" qualifier="sang" xml:lang="fr"><term>Hypersensibilité</term>
<term>Hypersensibilité respiratoire</term>
<term>Immunoglobuline E</term>
<term>Immunoglobuline G</term>
<term>Pneumopathie infectieuse</term>
</keywords>
<keywords scheme="MESH" xml:lang="en"><term>Animals</term>
<term>Hyperplasia</term>
<term>Mice, Inbred BALB C</term>
<term>Respiratory Mechanics</term>
</keywords>
<keywords scheme="MESH" xml:lang="fr"><term>Animaux</term>
<term>Hyperplasie</term>
<term>Mécanique respiratoire</term>
<term>Souris de lignée BALB C</term>
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<front><div type="abstract" xml:lang="en">Protein S-glutathionylation (PSSG) is an oxidant-induced post-translational modification of protein cysteines that impacts structure and function. The oxidoreductase glutaredoxin-1 (Glrx1) under physiological conditions catalyzes deglutathionylation and restores the protein thiol group. The involvement of Glrx1/PSSG in allergic inflammation induced by asthma-relevant allergens remains unknown. In the present study, we examined the impact of genetic ablation of Glrx1 in the pathogenesis of house dust mite (HDM)-induced allergic airways disease in mice. Wild-type (WT) or Glrx1(-/-) mice were instilled intranasally with HDM on 5 consecutive days for 3 weeks. As expected, overall PSSG was increased in Glrx1(-/-) HDM mice as compared with WT animals. Total cells in bronchoalveolar lavage fluid were similarly increased in HDM-treated WT and Glrx1(-/-) mice. However, in response to HDM, mice lacking Glrx1 demonstrated significantly more neutrophils and macrophages but fewer eosinophils as compared with HDM-exposed WT mice. mRNA expression of the Th2-associated cytokines IL-13 and IL-6, as well as mucin-5AC (Muc5ac), was significantly attenuated in Glrx1(-/-) HDM-treated mice. Conversely, mRNA expression of IFN-γ and IL-17A was increased in Glrx1(-/-) HDM mice compared with WT littermates. Restimulation of single-cell suspensions isolated from lungs or spleens with HDM resulted in enhanced IL-17A and decreased IL-5 production in cells derived from inflamed Glrx1(-/-) mice compared with WT animals. Finally, HDM-induced tissue damping and elastance were significantly attenuated in Glrx1(-/-) mice compared with WT littermates. These results demonstrate that the Glrx1-PSSG axis plays a pivotal role in HDM-induced allergic airways disease in association with enhanced type 2 inflammation and restriction of IFN-γ and IL-17A.</div>
</front>
</TEI>
<pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">27035878</PMID>
<DateCompleted><Year>2017</Year>
<Month>06</Month>
<Day>30</Day>
</DateCompleted>
<DateRevised><Year>2018</Year>
<Month>11</Month>
<Day>13</Day>
</DateRevised>
<Article PubModel="Print"><Journal><ISSN IssnType="Electronic">1535-4989</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>55</Volume>
<Issue>3</Issue>
<PubDate><Year>2016</Year>
<Month>09</Month>
</PubDate>
</JournalIssue>
<Title>American journal of respiratory cell and molecular biology</Title>
<ISOAbbreviation>Am J Respir Cell Mol Biol</ISOAbbreviation>
</Journal>
<ArticleTitle>Ablation of Glutaredoxin-1 Modulates House Dust Mite-Induced Allergic Airways Disease in Mice.</ArticleTitle>
<Pagination><MedlinePgn>377-86</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1165/rcmb.2015-0401OC</ELocationID>
<Abstract><AbstractText>Protein S-glutathionylation (PSSG) is an oxidant-induced post-translational modification of protein cysteines that impacts structure and function. The oxidoreductase glutaredoxin-1 (Glrx1) under physiological conditions catalyzes deglutathionylation and restores the protein thiol group. The involvement of Glrx1/PSSG in allergic inflammation induced by asthma-relevant allergens remains unknown. In the present study, we examined the impact of genetic ablation of Glrx1 in the pathogenesis of house dust mite (HDM)-induced allergic airways disease in mice. Wild-type (WT) or Glrx1(-/-) mice were instilled intranasally with HDM on 5 consecutive days for 3 weeks. As expected, overall PSSG was increased in Glrx1(-/-) HDM mice as compared with WT animals. Total cells in bronchoalveolar lavage fluid were similarly increased in HDM-treated WT and Glrx1(-/-) mice. However, in response to HDM, mice lacking Glrx1 demonstrated significantly more neutrophils and macrophages but fewer eosinophils as compared with HDM-exposed WT mice. mRNA expression of the Th2-associated cytokines IL-13 and IL-6, as well as mucin-5AC (Muc5ac), was significantly attenuated in Glrx1(-/-) HDM-treated mice. Conversely, mRNA expression of IFN-γ and IL-17A was increased in Glrx1(-/-) HDM mice compared with WT littermates. Restimulation of single-cell suspensions isolated from lungs or spleens with HDM resulted in enhanced IL-17A and decreased IL-5 production in cells derived from inflamed Glrx1(-/-) mice compared with WT animals. Finally, HDM-induced tissue damping and elastance were significantly attenuated in Glrx1(-/-) mice compared with WT littermates. These results demonstrate that the Glrx1-PSSG axis plays a pivotal role in HDM-induced allergic airways disease in association with enhanced type 2 inflammation and restriction of IFN-γ and IL-17A.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Hoffman</LastName>
<ForeName>Sidra M</ForeName>
<Initials>SM</Initials>
<AffiliationInfo><Affiliation>Departments of 1 Pathology and Laboratory Medicine and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Qian</LastName>
<ForeName>Xi</ForeName>
<Initials>X</Initials>
<AffiliationInfo><Affiliation>Departments of 1 Pathology and Laboratory Medicine and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Nolin</LastName>
<ForeName>James D</ForeName>
<Initials>JD</Initials>
<AffiliationInfo><Affiliation>Departments of 1 Pathology and Laboratory Medicine and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chapman</LastName>
<ForeName>David G</ForeName>
<Initials>DG</Initials>
<AffiliationInfo><Affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Chia</LastName>
<ForeName>Shi Biao</ForeName>
<Initials>SB</Initials>
<AffiliationInfo><Affiliation>Departments of 1 Pathology and Laboratory Medicine and.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Lahue</LastName>
<ForeName>Karolyn G</ForeName>
<Initials>KG</Initials>
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</AffiliationInfo>
</Author>
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<ForeName>Robert</ForeName>
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</Author>
<Author ValidYN="Y"><LastName>Ather</LastName>
<ForeName>Jennifer L</ForeName>
<Initials>JL</Initials>
<AffiliationInfo><Affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Randall</LastName>
<ForeName>Matthew J</ForeName>
<Initials>MJ</Initials>
<AffiliationInfo><Affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>McMillan</LastName>
<ForeName>David H</ForeName>
<Initials>DH</Initials>
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</AffiliationInfo>
</Author>
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<ForeName>Jane T</ForeName>
<Initials>JT</Initials>
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</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Taatjes</LastName>
<ForeName>Douglas J</ForeName>
<Initials>DJ</Initials>
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</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Aliyeva</LastName>
<ForeName>Minara</ForeName>
<Initials>M</Initials>
<AffiliationInfo><Affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Daphtary</LastName>
<ForeName>Nirav</ForeName>
<Initials>N</Initials>
<AffiliationInfo><Affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Abdalla</LastName>
<ForeName>Sarah</ForeName>
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</AffiliationInfo>
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<ForeName>Lennart K A</ForeName>
<Initials>LK</Initials>
<AffiliationInfo><Affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Ho</LastName>
<ForeName>Ye-Shih</ForeName>
<Initials>YS</Initials>
<AffiliationInfo><Affiliation>3 Institute of Environmental Health Sciences, Wayne State University, Detroit, Michigan; and.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Anathy</LastName>
<ForeName>Vikas</ForeName>
<Initials>V</Initials>
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</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Irvin</LastName>
<ForeName>Charles G</ForeName>
<Initials>CG</Initials>
<AffiliationInfo><Affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</Affiliation>
</AffiliationInfo>
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<Author ValidYN="Y"><LastName>Wouters</LastName>
<ForeName>Emiel F M</ForeName>
<Initials>EF</Initials>
<AffiliationInfo><Affiliation>4 Department of Respiratory Medicine, Maastricht University Medical Center, Maastricht, the Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Reynaert</LastName>
<ForeName>Niki L</ForeName>
<Initials>NL</Initials>
<AffiliationInfo><Affiliation>4 Department of Respiratory Medicine, Maastricht University Medical Center, Maastricht, the Netherlands.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Dixon</LastName>
<ForeName>Anne E</ForeName>
<Initials>AE</Initials>
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</AffiliationInfo>
</Author>
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<Initials>A</Initials>
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</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Poynter</LastName>
<ForeName>Matthew E</ForeName>
<Initials>ME</Initials>
<AffiliationInfo><Affiliation>2 Medicine, University of Vermont, Burlington, Vermont.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Janssen-Heininger</LastName>
<ForeName>Yvonne M W</ForeName>
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<AffiliationInfo><Affiliation>Departments of 1 Pathology and Laboratory Medicine and.</Affiliation>
</AffiliationInfo>
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<Language>eng</Language>
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<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
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<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
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<Acronym>HL</Acronym>
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<Country>United States</Country>
</Grant>
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<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
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<Acronym>GM</Acronym>
<Agency>NIGMS NIH HHS</Agency>
<Country>United States</Country>
</Grant>
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<Acronym>HL</Acronym>
<Agency>NHLBI NIH HHS</Agency>
<Country>United States</Country>
</Grant>
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<Acronym>ES</Acronym>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D016207" MajorTopicYN="N">Cytokines</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName>
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</MeshHeading>
<MeshHeading><DescriptorName UI="D054477" MajorTopicYN="N">Glutaredoxins</DescriptorName>
<QualifierName UI="Q000378" MajorTopicYN="Y">metabolism</QualifierName>
</MeshHeading>
<MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName>
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