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Redox-active protein thioredoxin-1 administration ameliorates influenza A virus (H1N1)-induced acute lung injury in mice.

Identifieur interne : 000545 ( PubMed/Corpus ); précédent : 000544; suivant : 000546

Redox-active protein thioredoxin-1 administration ameliorates influenza A virus (H1N1)-induced acute lung injury in mice.

Auteurs : Masato Yashiro ; Hirokazu Tsukahara ; Akihiro Matsukawa ; Mutsuko Yamada ; Yosuke Fujii ; Yoshiharu Nagaoka ; Mitsuru Tsuge ; Nobuko Yamashita ; Toshihiro Ito ; Masao Yamada ; Hiroshi Masutani ; Junji Yodoi ; Tsuneo Morishima

Source :

RBID : pubmed:23222257

English descriptors

Abstract

Influenza virus infections can cause severe acute lung injury leading to significant morbidity and mortality. Thioredoxin-1 is a redox-active defensive protein induced in response to stress conditions. Animal experiments have revealed that thioredoxin-1 has protective effects against various severe disorders. This study was undertaken to evaluate the protective effects of recombinant human thioredoxin-1 administration on influenza A virus (H1N1)-induced acute lung injury in mice.

DOI: 10.1097/CCM.0b013e3182676352
PubMed: 23222257

Links to Exploration step

pubmed:23222257

Le document en format XML

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<term>Acute Lung Injury (drug therapy)</term>
<term>Acute Lung Injury (immunology)</term>
<term>Acute Lung Injury (pathology)</term>
<term>Acute Lung Injury (virology)</term>
<term>Animals</term>
<term>Antioxidants (pharmacology)</term>
<term>Antioxidants (therapeutic use)</term>
<term>Chemokine CXCL1 (drug effects)</term>
<term>Chemokine CXCL1 (metabolism)</term>
<term>Humans</term>
<term>Influenza A Virus, H1N1 Subtype</term>
<term>Influenza, Human (drug therapy)</term>
<term>Male</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Neutrophil Infiltration (drug effects)</term>
<term>Pneumonia, Viral (drug therapy)</term>
<term>Prospective Studies</term>
<term>Recombinant Proteins (pharmacology)</term>
<term>Recombinant Proteins (therapeutic use)</term>
<term>Survival Analysis</term>
<term>Thioredoxins (pharmacology)</term>
<term>Thioredoxins (therapeutic use)</term>
<term>Tumor Necrosis Factor-alpha (drug effects)</term>
<term>Tumor Necrosis Factor-alpha (metabolism)</term>
<term>Viral Load (drug effects)</term>
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<term>Tumor Necrosis Factor-alpha</term>
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<term>Antioxidants</term>
<term>Recombinant Proteins</term>
<term>Thioredoxins</term>
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<term>Neutrophil Infiltration</term>
<term>Viral Load</term>
</keywords>
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<term>Acute Lung Injury</term>
<term>Influenza, Human</term>
<term>Pneumonia, Viral</term>
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<term>Acute Lung Injury</term>
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<term>Recombinant Proteins</term>
<term>Thioredoxins</term>
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<term>Acute Lung Injury</term>
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<term>Humans</term>
<term>Influenza A Virus, H1N1 Subtype</term>
<term>Male</term>
<term>Mice</term>
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<div type="abstract" xml:lang="en">Influenza virus infections can cause severe acute lung injury leading to significant morbidity and mortality. Thioredoxin-1 is a redox-active defensive protein induced in response to stress conditions. Animal experiments have revealed that thioredoxin-1 has protective effects against various severe disorders. This study was undertaken to evaluate the protective effects of recombinant human thioredoxin-1 administration on influenza A virus (H1N1)-induced acute lung injury in mice.</div>
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<Month>03</Month>
<Day>04</Day>
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<Year>2019</Year>
<Month>12</Month>
<Day>10</Day>
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<Volume>41</Volume>
<Issue>1</Issue>
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<Year>2013</Year>
<Month>Jan</Month>
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<Title>Critical care medicine</Title>
<ISOAbbreviation>Crit. Care Med.</ISOAbbreviation>
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<ArticleTitle>Redox-active protein thioredoxin-1 administration ameliorates influenza A virus (H1N1)-induced acute lung injury in mice.</ArticleTitle>
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<AbstractText Label="OBJECTIVES" NlmCategory="OBJECTIVE">Influenza virus infections can cause severe acute lung injury leading to significant morbidity and mortality. Thioredoxin-1 is a redox-active defensive protein induced in response to stress conditions. Animal experiments have revealed that thioredoxin-1 has protective effects against various severe disorders. This study was undertaken to evaluate the protective effects of recombinant human thioredoxin-1 administration on influenza A virus (H1N1)-induced acute lung injury in mice.</AbstractText>
<AbstractText Label="DESIGN" NlmCategory="METHODS">Prospective animal trial.</AbstractText>
<AbstractText Label="SETTING" NlmCategory="METHODS">Research laboratory.</AbstractText>
<AbstractText Label="SUBJECTS" NlmCategory="METHODS">Nine-week-old male C57BL/6 mice inoculated with H1N1.</AbstractText>
<AbstractText Label="INTERVENTION" NlmCategory="METHODS">The mice were divided into a vehicle-treated group and recombinant human thioredoxin-1-treated group. For survival rate analysis, the vehicle or recombinant human thioredoxin-1 was administered intraperitoneally every second day from day -1 to day 13. For lung lavage and pathological analyses, vehicle or recombinant human thioredoxin-1 was administered intraperitoneally on days -1, 1, and 3.</AbstractText>
<AbstractText Label="MEASUREMENTS AND MAIN RESULTS" NlmCategory="RESULTS">Lung lavage and pathological analyses were performed at 24, 72, and 120 hrs after inoculation. The recombinant human thioredoxin-1 treatment significantly improved the survival rate of H1N1-inoculated mice, although the treatment did not affect virus propagation in the lung. The treatment significantly attenuated the histological changes and neutrophil infiltration in the lung of H1N1-inoculated mice. The treatment significantly attenuated the production of tumor necrosis factor-α and chemokine (C-X-C motif) ligand 1 in the lung and oxidative stress enhancement, which were observed in H1N1-inoculated mice. H1N1 induced expressions of tumor necrosis factor-α and chemokine (C-X-C motif) ligand 1 in murine lung epithelial cells MLE-12, which were inhibited by the addition of recombinant human thioredoxin-1. The recombinant human thioredoxin-1 treatment started 30 mins after H1N1 inoculation also significantly improved the survival of the mice.</AbstractText>
<AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Exogenous administration of recombinant human thioredoxin-1 significantly improved the survival rate and attenuated lung histological changes in the murine model of influenza pneumonia. The protective mechanism of thioredoxin-1 might be explained by its potent antioxidative and anti-inflammatory actions. Consequently, recombinant human thioredoxin-1 might be a possible pharmacological strategy for severe influenza virus infection in humans.</AbstractText>
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