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The Flavonoid Isoliquiritigenin Reduces Lung Inflammation and Mouse Morbidity during Influenza Virus Infection.

Identifieur interne : 000407 ( PubMed/Curation ); précédent : 000406; suivant : 000408

The Flavonoid Isoliquiritigenin Reduces Lung Inflammation and Mouse Morbidity during Influenza Virus Infection.

Auteurs : Hussein Traboulsi [Canada] ; Alexandre Cloutier [Canada] ; Kumaraswamy Boyapelly [Canada] ; Marc-André Bonin [Canada] ; Éric Marsault [Canada] ; André M. Cantin [Canada] ; Martin V. Richter [Canada]

Source :

Antimicrobial agents and chemotherapy [ 1098-6596 ] ; 2015.

RBID : pubmed:26248373

Descripteurs français

English descriptors

KwdEn :
- Animals, Anti-Inflammatory Agents (pharmacology), Antiviral Agents (pharmacology), CD8-Positive T-Lymphocytes (drug effects), CD8-Positive T-Lymphocytes (immunology), CD8-Positive T-Lymphocytes (virology), Cell Line, Chalcones (pharmacology), Chemokine CCL5 (genetics), Chemokine CCL5 (immunology), Epithelial Cells (drug effects), Epithelial Cells (immunology), Epithelial Cells (virology), Gene Expression Regulation, Humans, Influenza A Virus, H1N1 Subtype (drug effects), Influenza A Virus, H1N1 Subtype (growth & development), Interferon-gamma (genetics), Interferon-gamma (immunology), Interleukin-1beta (genetics), Interleukin-1beta (immunology), Interleukin-6 (genetics), Interleukin-6 (immunology), Lung (drug effects), Lung (immunology), Lung (pathology), Lung (virology), Mice, Mice, Inbred C57BL, Orthomyxoviridae Infections (drug therapy), Orthomyxoviridae Infections (immunology), Orthomyxoviridae Infections (pathology), Orthomyxoviridae Infections (virology), PPAR gamma (genetics), PPAR gamma (immunology), Pneumonia (drug therapy), Pneumonia (immunology), Pneumonia (pathology), Pneumonia (virology), Signal Transduction, Tumor Necrosis Factor-alpha (genetics), Tumor Necrosis Factor-alpha (immunology), Viral Load (drug effects), Virus Replication (drug effects).
MESH :
- chemical , genetics : Chemokine CCL5, Interferon-gamma, Interleukin-1beta, Interleukin-6, PPAR gamma, Tumor Necrosis Factor-alpha.
- chemical , immunology : Chemokine CCL5, Interferon-gamma, Interleukin-1beta, Interleukin-6, PPAR gamma, Tumor Necrosis Factor-alpha.
- chemical , pharmacology : Anti-Inflammatory Agents, Antiviral Agents, Chalcones.
- drug effects : CD8-Positive T-Lymphocytes, Epithelial Cells, Influenza A Virus, H1N1 Subtype, Lung, Viral Load, Virus Replication.
- drug therapy : Orthomyxoviridae Infections, Pneumonia.
- growth & development : Influenza A Virus, H1N1 Subtype.
- immunology : CD8-Positive T-Lymphocytes, Epithelial Cells, Lung, Orthomyxoviridae Infections, Pneumonia.
- pathology : Lung, Orthomyxoviridae Infections, Pneumonia.
- virology : CD8-Positive T-Lymphocytes, Epithelial Cells, Lung, Orthomyxoviridae Infections, Pneumonia.
- Animals, Cell Line, Gene Expression Regulation, Humans, Mice, Mice, Inbred C57BL, Signal Transduction.

Abstract

The host response to influenza virus infection is characterized by an acute lung inflammatory response in which intense inflammatory cell recruitment, hypercytokinemia, and a high level of oxidative stress are present. The sum of these events contributes to the virus-induced lung damage that leads to high a level of morbidity and mortality in susceptible infected patients. In this context, we identified compounds that can simultaneously reduce the excessive inflammatory response and the viral replication as a strategy to treat influenza virus infection. We investigated the anti-inflammatory and antiviral potential activities of isoliquiritigenin (ILG). Interestingly, we demonstrated that ILG is a potent inhibitor of influenza virus replication in human bronchial epithelial cells (50% effective concentration [EC50] = 24.7 μM). In addition, our results showed that this molecule inhibits the expression of inflammatory cytokines induced after the infection of cells with influenza virus. We demonstrated that the anti-inflammatory activity of ILG in the context of influenza virus infection is dependent on the activation of the peroxisome proliferator-activated receptor gamma pathway. Interestingly, ILG phosphate (ILG-p)-treated mice displayed decreased lung inflammation as depicted by reduced cytokine gene expression and inflammatory cell recruitment. We also demonstrated that influenza virus-specific CD8(+) effector T cell recruitment was reduced up to 60% in the lungs of mice treated with ILG-p (10 mg/kg) compared to that in saline-treated mice. Finally, we showed that administration of ILG-p reduced lung viral titers and morbidity of mice infected with the PR8/H1N1 virus.

DOI: 10.1128/AAC.01098-15
PubMed: 26248373

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<term>Anti-Inflammatory Agents (pharmacology)</term>
<term>Antiviral Agents (pharmacology)</term>
<term>CD8-Positive T-Lymphocytes (drug effects)</term>
<term>CD8-Positive T-Lymphocytes (immunology)</term>
<term>CD8-Positive T-Lymphocytes (virology)</term>
<term>Cell Line</term>
<term>Chalcones (pharmacology)</term>
<term>Chemokine CCL5 (genetics)</term>
<term>Chemokine CCL5 (immunology)</term>
<term>Epithelial Cells (drug effects)</term>
<term>Epithelial Cells (immunology)</term>
<term>Epithelial Cells (virology)</term>
<term>Gene Expression Regulation</term>
<term>Humans</term>
<term>Influenza A Virus, H1N1 Subtype (drug effects)</term>
<term>Influenza A Virus, H1N1 Subtype (growth & development)</term>
<term>Interferon-gamma (genetics)</term>
<term>Interferon-gamma (immunology)</term>
<term>Interleukin-1beta (genetics)</term>
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<term>Interleukin-6 (genetics)</term>
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<term>Lung (immunology)</term>
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<term>Antiviraux (pharmacologie)</term>
<term>Cellules épithéliales ()</term>
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<term>Chimiokine CCL5 (génétique)</term>
<term>Chimiokine CCL5 (immunologie)</term>
<term>Facteur de nécrose tumorale alpha (génétique)</term>
<term>Facteur de nécrose tumorale alpha (immunologie)</term>
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<term>Infections à Orthomyxoviridae (anatomopathologie)</term>
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<term>Interleukin-1beta</term>
<term>Interleukin-6</term>
<term>PPAR gamma</term>
<term>Tumor Necrosis Factor-alpha</term>
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<term>Interferon-gamma</term>
<term>Interleukin-1beta</term>
<term>Interleukin-6</term>
<term>PPAR gamma</term>
<term>Tumor Necrosis Factor-alpha</term>
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<term>Antiviral Agents</term>
<term>Chalcones</term>
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<term>Pneumopathie infectieuse</term>
<term>Poumon</term>
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<term>Epithelial Cells</term>
<term>Influenza A Virus, H1N1 Subtype</term>
<term>Lung</term>
<term>Viral Load</term>
<term>Virus Replication</term>
</keywords>
<keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Orthomyxoviridae Infections</term>
<term>Pneumonia</term>
</keywords>
<keywords scheme="MESH" qualifier="growth & development" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term>
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<term>Facteur de nécrose tumorale alpha</term>
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<term>Interleukine-1 bêta</term>
<term>Interleukine-6</term>
<term>Récepteur PPAR gamma</term>
</keywords>
<keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Cellules épithéliales</term>
<term>Chimiokine CCL5</term>
<term>Facteur de nécrose tumorale alpha</term>
<term>Infections à Orthomyxoviridae</term>
<term>Interféron gamma</term>
<term>Interleukine-1 bêta</term>
<term>Interleukine-6</term>
<term>Lymphocytes T CD8+</term>
<term>Pneumopathie infectieuse</term>
<term>Poumon</term>
<term>Récepteur PPAR gamma</term>
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<keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>CD8-Positive T-Lymphocytes</term>
<term>Epithelial Cells</term>
<term>Lung</term>
<term>Orthomyxoviridae Infections</term>
<term>Pneumonia</term>
</keywords>
<keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Lung</term>
<term>Orthomyxoviridae Infections</term>
<term>Pneumonia</term>
</keywords>
<keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Anti-inflammatoires</term>
<term>Antiviraux</term>
<term>Chalcones</term>
</keywords>
<keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Infections à Orthomyxoviridae</term>
<term>Pneumopathie infectieuse</term>
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<term>Infections à Orthomyxoviridae</term>
<term>Lymphocytes T CD8+</term>
<term>Pneumopathie infectieuse</term>
<term>Poumon</term>
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<term>Epithelial Cells</term>
<term>Lung</term>
<term>Orthomyxoviridae Infections</term>
<term>Pneumonia</term>
</keywords>
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<term>Cell Line</term>
<term>Gene Expression Regulation</term>
<term>Humans</term>
<term>Mice</term>
<term>Mice, Inbred C57BL</term>
<term>Signal Transduction</term>
</keywords>
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<term>Cellules épithéliales</term>
<term>Charge virale</term>
<term>Humains</term>
<term>Lignée cellulaire</term>
<term>Lymphocytes T CD8+</term>
<term>Poumon</term>
<term>Régulation de l'expression des gènes</term>
<term>Réplication virale</term>
<term>Souris</term>
<term>Souris de lignée C57BL</term>
<term>Sous-type H1N1 du virus de la grippe A</term>
<term>Transduction du signal</term>
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<front><div type="abstract" xml:lang="en">The host response to influenza virus infection is characterized by an acute lung inflammatory response in which intense inflammatory cell recruitment, hypercytokinemia, and a high level of oxidative stress are present. The sum of these events contributes to the virus-induced lung damage that leads to high a level of morbidity and mortality in susceptible infected patients. In this context, we identified compounds that can simultaneously reduce the excessive inflammatory response and the viral replication as a strategy to treat influenza virus infection. We investigated the anti-inflammatory and antiviral potential activities of isoliquiritigenin (ILG). Interestingly, we demonstrated that ILG is a potent inhibitor of influenza virus replication in human bronchial epithelial cells (50% effective concentration [EC50] = 24.7 μM). In addition, our results showed that this molecule inhibits the expression of inflammatory cytokines induced after the infection of cells with influenza virus. We demonstrated that the anti-inflammatory activity of ILG in the context of influenza virus infection is dependent on the activation of the peroxisome proliferator-activated receptor gamma pathway. Interestingly, ILG phosphate (ILG-p)-treated mice displayed decreased lung inflammation as depicted by reduced cytokine gene expression and inflammatory cell recruitment. We also demonstrated that influenza virus-specific CD8(+) effector T cell recruitment was reduced up to 60% in the lungs of mice treated with ILG-p (10 mg/kg) compared to that in saline-treated mice. Finally, we showed that administration of ILG-p reduced lung viral titers and morbidity of mice infected with the PR8/H1N1 virus. </div>
</front>
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<DateCompleted><Year>2016</Year>
<Month>06</Month>
<Day>15</Day>
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<DateRevised><Year>2018</Year>
<Month>11</Month>
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<Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1098-6596</ISSN>
<JournalIssue CitedMedium="Internet"><Volume>59</Volume>
<Issue>10</Issue>
<PubDate><Year>2015</Year>
<Month>Oct</Month>
</PubDate>
</JournalIssue>
<Title>Antimicrobial agents and chemotherapy</Title>
<ISOAbbreviation>Antimicrob. Agents Chemother.</ISOAbbreviation>
</Journal>
<ArticleTitle>The Flavonoid Isoliquiritigenin Reduces Lung Inflammation and Mouse Morbidity during Influenza Virus Infection.</ArticleTitle>
<Pagination><MedlinePgn>6317-27</MedlinePgn>
</Pagination>
<ELocationID EIdType="doi" ValidYN="Y">10.1128/AAC.01098-15</ELocationID>
<Abstract><AbstractText>The host response to influenza virus infection is characterized by an acute lung inflammatory response in which intense inflammatory cell recruitment, hypercytokinemia, and a high level of oxidative stress are present. The sum of these events contributes to the virus-induced lung damage that leads to high a level of morbidity and mortality in susceptible infected patients. In this context, we identified compounds that can simultaneously reduce the excessive inflammatory response and the viral replication as a strategy to treat influenza virus infection. We investigated the anti-inflammatory and antiviral potential activities of isoliquiritigenin (ILG). Interestingly, we demonstrated that ILG is a potent inhibitor of influenza virus replication in human bronchial epithelial cells (50% effective concentration [EC50] = 24.7 μM). In addition, our results showed that this molecule inhibits the expression of inflammatory cytokines induced after the infection of cells with influenza virus. We demonstrated that the anti-inflammatory activity of ILG in the context of influenza virus infection is dependent on the activation of the peroxisome proliferator-activated receptor gamma pathway. Interestingly, ILG phosphate (ILG-p)-treated mice displayed decreased lung inflammation as depicted by reduced cytokine gene expression and inflammatory cell recruitment. We also demonstrated that influenza virus-specific CD8(+) effector T cell recruitment was reduced up to 60% in the lungs of mice treated with ILG-p (10 mg/kg) compared to that in saline-treated mice. Finally, we showed that administration of ILG-p reduced lung viral titers and morbidity of mice infected with the PR8/H1N1 virus. </AbstractText>
<CopyrightInformation>Copyright © 2015, American Society for Microbiology. All Rights Reserved.</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Traboulsi</LastName>
<ForeName>Hussein</ForeName>
<Initials>H</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, Pulmonary Division, Faculty of Medicine and Health Sciences, Université de Sherbrooke, and Centre de recherche du CHUS, Sherbrooke, Québec, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cloutier</LastName>
<ForeName>Alexandre</ForeName>
<Initials>A</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, Pulmonary Division, Faculty of Medicine and Health Sciences, Université de Sherbrooke, and Centre de recherche du CHUS, Sherbrooke, Québec, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Boyapelly</LastName>
<ForeName>Kumaraswamy</ForeName>
<Initials>K</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology-Physiology, Faculty of Medicine and Health Sciences, Université de Sherbrooke, and Institut de Pharmacologie de Sherbrooke, Sherbooke, Québec, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Bonin</LastName>
<ForeName>Marc-André</ForeName>
<Initials>MA</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology-Physiology, Faculty of Medicine and Health Sciences, Université de Sherbrooke, and Institut de Pharmacologie de Sherbrooke, Sherbooke, Québec, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Marsault</LastName>
<ForeName>Éric</ForeName>
<Initials>É</Initials>
<AffiliationInfo><Affiliation>Department of Pharmacology-Physiology, Faculty of Medicine and Health Sciences, Université de Sherbrooke, and Institut de Pharmacologie de Sherbrooke, Sherbooke, Québec, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Cantin</LastName>
<ForeName>André M</ForeName>
<Initials>AM</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, Pulmonary Division, Faculty of Medicine and Health Sciences, Université de Sherbrooke, and Centre de recherche du CHUS, Sherbrooke, Québec, Canada.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y"><LastName>Richter</LastName>
<ForeName>Martin V</ForeName>
<Initials>MV</Initials>
<AffiliationInfo><Affiliation>Department of Medicine, Pulmonary Division, Faculty of Medicine and Health Sciences, Université de Sherbrooke, and Centre de recherche du CHUS, Sherbrooke, Québec, Canada Martin.Richter@USherbrooke.ca.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>eng</Language>
<PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
<ArticleDate DateType="Electronic"><Year>2015</Year>
<Month>07</Month>
<Day>27</Day>
</ArticleDate>
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<MedlineTA>Antimicrob Agents Chemother</MedlineTA>
<NlmUniqueID>0315061</NlmUniqueID>
<ISSNLinking>0066-4804</ISSNLinking>
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</MeshHeading>
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The Flavonoid Isoliquiritigenin Reduces Lung Inflammation and Mouse Morbidity during Influenza Virus Infection.

The Flavonoid Isoliquiritigenin Reduces Lung Inflammation and Mouse Morbidity during Influenza Virus Infection.

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