Apocynin and ebselen reduce influenza A virus-induced lung inflammation in cigarette smoke-exposed mice.
Identifieur interne : 000B99 ( Main/Exploration ); précédent : 000B98; suivant : 000C00Apocynin and ebselen reduce influenza A virus-induced lung inflammation in cigarette smoke-exposed mice.
Auteurs : L C Oostwoud [Australie] ; P. Gunasinghe [Australie] ; H J Seow [Australie] ; J M Ye [Australie] ; S. Selemidis [Australie] ; S. Bozinovski [Australie] ; R. Vlahos [Australie]Source :
- Scientific reports [ 2045-2322 ] ; 2016.
Descripteurs français
- KwdFr :
- Acétophénones (administration et posologie), Animaux, Azoles (administration et posologie), Broncho-pneumopathie chronique obstructive (anatomopathologie), Broncho-pneumopathie chronique obstructive (traitement médicamenteux), Broncho-pneumopathie chronique obstructive (virologie), Composés organiques du sélénium (administration et posologie), Fumée (effets indésirables), Humains, Modèles animaux de maladie humaine, Mâle, Pneumopathie infectieuse (anatomopathologie), Pneumopathie infectieuse (traitement médicamenteux), Pneumopathie infectieuse (virologie), Souris, Stress oxydatif (), Tabac (effets indésirables), Tabagisme (effets indésirables), Virus de la grippe A (), Virus de la grippe A (pathogénicité).
- MESH :
- administration et posologie : Acétophénones, Azoles, Composés organiques du sélénium.
- anatomopathologie : Broncho-pneumopathie chronique obstructive, Pneumopathie infectieuse.
- effets indésirables : Fumée, Tabac, Tabagisme.
- pathogénicité : Virus de la grippe A.
- traitement médicamenteux : Broncho-pneumopathie chronique obstructive, Pneumopathie infectieuse.
- virologie : Broncho-pneumopathie chronique obstructive, Pneumopathie infectieuse.
- Animaux, Humains, Modèles animaux de maladie humaine, Mâle, Souris, Stress oxydatif, Virus de la grippe A.
English descriptors
- KwdEn :
- Acetophenones (administration & dosage), Animals, Azoles (administration & dosage), Disease Models, Animal, Humans, Influenza A virus (drug effects), Influenza A virus (pathogenicity), Male, Mice, Organoselenium Compounds (administration & dosage), Oxidative Stress (drug effects), Pneumonia (drug therapy), Pneumonia (pathology), Pneumonia (virology), Pulmonary Disease, Chronic Obstructive (drug therapy), Pulmonary Disease, Chronic Obstructive (pathology), Pulmonary Disease, Chronic Obstructive (virology), Smoke (adverse effects), Smoking (adverse effects), Tobacco (adverse effects).
- MESH :
- chemical , administration & dosage : Acetophenones, Azoles, Organoselenium Compounds.
- chemical , adverse effects : Smoke.
- adverse effects : Smoking, Tobacco.
- drug effects : Influenza A virus, Oxidative Stress.
- drug therapy : Pneumonia, Pulmonary Disease, Chronic Obstructive.
- pathogenicity : Influenza A virus.
- pathology : Pneumonia, Pulmonary Disease, Chronic Obstructive.
- virology : Pneumonia, Pulmonary Disease, Chronic Obstructive.
- Animals, Disease Models, Animal, Humans, Male, Mice.
Abstract
Influenza A virus (IAV) infections are a common cause of acute exacerbations of chronic obstructive pulmonary disease (AECOPD). Oxidative stress is increased in COPD, IAV-induced lung inflammation and AECOPD. Therefore, we investigated whether targeting oxidative stress with the Nox2 oxidase inhibitors and ROS scavengers, apocynin and ebselen could ameliorate lung inflammation in a mouse model of AECOPD. Male BALB/c mice were exposed to cigarette smoke (CS) generated from 9 cigarettes per day for 4 days. On day 5, mice were infected with 1 × 10(4.5) PFUs of the IAV Mem71 (H3N1). BALF inflammation, viral titers, superoxide production and whole lung cytokine, chemokine and protease mRNA expression were assessed 3 and 7 days post infection. IAV infection resulted in a greater increase in BALF inflammation in mice that had been exposed to CS compared to non-smoking mice. This increase in BALF inflammation in CS-exposed mice caused by IAV infection was associated with elevated gene expression of pro-inflammatory cytokines, chemokines and proteases, compared to CS alone mice. Apocynin and ebselen significantly reduced the exacerbated BALF inflammation and pro-inflammatory cytokine, chemokine and protease expression caused by IAV infection in CS mice. Targeting oxidative stress using apocynin and ebselen reduces IAV-induced lung inflammation in CS-exposed mice and may be therapeutically exploited to alleviate AECOPD.
DOI: 10.1038/srep20983
PubMed: 26877172
Affiliations:
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Le document en format XML
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Animal</term><term>Humans</term><term>Influenza A virus (drug effects)</term><term>Influenza A virus (pathogenicity)</term><term>Male</term><term>Mice</term><term>Organoselenium Compounds (administration & dosage)</term><term>Oxidative Stress (drug effects)</term><term>Pneumonia (drug therapy)</term><term>Pneumonia (pathology)</term><term>Pneumonia (virology)</term><term>Pulmonary Disease, Chronic Obstructive (drug therapy)</term><term>Pulmonary Disease, Chronic Obstructive (pathology)</term><term>Pulmonary Disease, Chronic Obstructive (virology)</term><term>Smoke (adverse effects)</term><term>Smoking (adverse effects)</term><term>Tobacco (adverse effects)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Acétophénones (administration et posologie)</term><term>Animaux</term><term>Azoles (administration et posologie)</term><term>Broncho-pneumopathie chronique obstructive (anatomopathologie)</term><term>Broncho-pneumopathie chronique obstructive (traitement médicamenteux)</term><term>Broncho-pneumopathie chronique obstructive (virologie)</term><term>Composés organiques du sélénium (administration et posologie)</term><term>Fumée (effets indésirables)</term><term>Humains</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Pneumopathie infectieuse (anatomopathologie)</term><term>Pneumopathie infectieuse (traitement médicamenteux)</term><term>Pneumopathie infectieuse (virologie)</term><term>Souris</term><term>Stress oxydatif ()</term><term>Tabac (effets indésirables)</term><term>Tabagisme (effets indésirables)</term><term>Virus de la grippe A ()</term><term>Virus de la grippe A (pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Acetophenones</term><term>Azoles</term><term>Organoselenium Compounds</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Smoke</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Acétophénones</term><term>Azoles</term><term>Composés organiques du sélénium</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Smoking</term><term>Tobacco</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Broncho-pneumopathie chronique obstructive</term><term>Pneumopathie infectieuse</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Influenza A virus</term><term>Oxidative Stress</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Pneumonia</term><term>Pulmonary Disease, Chronic Obstructive</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Fumée</term><term>Tabac</term><term>Tabagisme</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus de la grippe A</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Pneumonia</term><term>Pulmonary Disease, Chronic Obstructive</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Broncho-pneumopathie chronique obstructive</term><term>Pneumopathie infectieuse</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Broncho-pneumopathie chronique obstructive</term><term>Pneumopathie infectieuse</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Pneumonia</term><term>Pulmonary Disease, Chronic Obstructive</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Humans</term><term>Male</term><term>Mice</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Humains</term><term>Modèles animaux de maladie humaine</term><term>Mâle</term><term>Souris</term><term>Stress oxydatif</term><term>Virus de la grippe A</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Influenza A virus (IAV) infections are a common cause of acute exacerbations of chronic obstructive pulmonary disease (AECOPD). Oxidative stress is increased in COPD, IAV-induced lung inflammation and AECOPD. Therefore, we investigated whether targeting oxidative stress with the Nox2 oxidase inhibitors and ROS scavengers, apocynin and ebselen could ameliorate lung inflammation in a mouse model of AECOPD. Male BALB/c mice were exposed to cigarette smoke (CS) generated from 9 cigarettes per day for 4 days. On day 5, mice were infected with 1 × 10(4.5) PFUs of the IAV Mem71 (H3N1). BALF inflammation, viral titers, superoxide production and whole lung cytokine, chemokine and protease mRNA expression were assessed 3 and 7 days post infection. IAV infection resulted in a greater increase in BALF inflammation in mice that had been exposed to CS compared to non-smoking mice. This increase in BALF inflammation in CS-exposed mice caused by IAV infection was associated with elevated gene expression of pro-inflammatory cytokines, chemokines and proteases, compared to CS alone mice. Apocynin and ebselen significantly reduced the exacerbated BALF inflammation and pro-inflammatory cytokine, chemokine and protease expression caused by IAV infection in CS mice. Targeting oxidative stress using apocynin and ebselen reduces IAV-induced lung inflammation in CS-exposed mice and may be therapeutically exploited to alleviate AECOPD.</div></front></TEI><affiliations><list><country><li>Australie</li></country><region><li>Victoria (État)</li></region><settlement><li>Melbourne</li></settlement><orgName><li>Université de Melbourne</li></orgName></list><tree><country name="Australie"><region name="Victoria (État)"><name sortKey="Oostwoud, L C" sort="Oostwoud, L C" uniqKey="Oostwoud L" first="L C" last="Oostwoud">L C Oostwoud</name></region><name sortKey="Bozinovski, S" sort="Bozinovski, S" uniqKey="Bozinovski S" first="S" last="Bozinovski">S. Bozinovski</name><name sortKey="Gunasinghe, P" sort="Gunasinghe, P" uniqKey="Gunasinghe P" first="P" last="Gunasinghe">P. Gunasinghe</name><name sortKey="Selemidis, S" sort="Selemidis, S" uniqKey="Selemidis S" first="S" last="Selemidis">S. Selemidis</name><name sortKey="Seow, H J" sort="Seow, H J" uniqKey="Seow H" first="H J" last="Seow">H J Seow</name><name sortKey="Vlahos, R" sort="Vlahos, R" uniqKey="Vlahos R" first="R" last="Vlahos">R. Vlahos</name><name sortKey="Ye, J M" sort="Ye, J M" uniqKey="Ye J" first="J M" last="Ye">J M Ye</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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