Chronic alcohol consumption increases the severity of murine influenza virus infections.
Identifieur interne : 000258 ( PubMed/Curation ); précédent : 000257; suivant : 000259Chronic alcohol consumption increases the severity of murine influenza virus infections.
Auteurs : David K. Meyerholz [États-Unis] ; Michelle Edsen-Moore ; Jodi Mcgill ; Ruth A. Coleman ; Robert T. Cook ; Kevin L. LeggeSource :
- Journal of immunology (Baltimore, Md. : 1950) [ 0022-1767 ] ; 2008.
Descripteurs français
- KwdFr :
- Animaux, Consommation d'alcool (physiopathologie), Facteurs temps, Femelle, Granulocytes neutrophiles (cytologie), Granulocytes neutrophiles (immunologie), Infections à Orthomyxoviridae (anatomopathologie), Infections à Orthomyxoviridae (immunologie), Infections à Orthomyxoviridae (virologie), Interféron gamma (biosynthèse), Lymphocytes T CD8+ (immunologie), Lymphocytes T CD8+ (métabolisme), Maladies pulmonaires (anatomopathologie), Mouvement cellulaire (immunologie), Souris, Sous-type H1N1 du virus de la grippe A (physiologie), Sous-type H2N2 du virus de la grippe A (physiologie), Taux de survie.
- MESH :
- anatomopathologie : Infections à Orthomyxoviridae, Maladies pulmonaires.
- biosynthèse : Interféron gamma.
- cytologie : Granulocytes neutrophiles.
- immunologie : Granulocytes neutrophiles, Infections à Orthomyxoviridae, Lymphocytes T CD8+, Mouvement cellulaire.
- métabolisme : Lymphocytes T CD8+.
- physiologie : Sous-type H1N1 du virus de la grippe A, Sous-type H2N2 du virus de la grippe A.
- physiopathologie : Consommation d'alcool.
- virologie : Infections à Orthomyxoviridae.
- Animaux, Facteurs temps, Femelle, Souris, Taux de survie.
English descriptors
- KwdEn :
- Alcohol Drinking (physiopathology), Animals, CD8-Positive T-Lymphocytes (immunology), CD8-Positive T-Lymphocytes (metabolism), Cell Movement (immunology), Female, Influenza A Virus, H1N1 Subtype (physiology), Influenza A Virus, H2N2 Subtype (physiology), Interferon-gamma (biosynthesis), Lung Diseases (pathology), Mice, Neutrophils (cytology), Neutrophils (immunology), Orthomyxoviridae Infections (immunology), Orthomyxoviridae Infections (pathology), Orthomyxoviridae Infections (virology), Survival Rate, Time Factors.
- MESH :
- chemical , biosynthesis : Interferon-gamma.
- cytology : Neutrophils.
- immunology : CD8-Positive T-Lymphocytes, Cell Movement, Neutrophils, Orthomyxoviridae Infections.
- metabolism : CD8-Positive T-Lymphocytes.
- pathology : Lung Diseases, Orthomyxoviridae Infections.
- physiology : Influenza A Virus, H1N1 Subtype, Influenza A Virus, H2N2 Subtype.
- physiopathology : Alcohol Drinking.
- virology : Orthomyxoviridae Infections.
- Animals, Female, Mice, Survival Rate, Time Factors.
Abstract
Respiratory infections with both seasonal as well as potential pandemic Influenza viruses represent a significant burden on human health. Furthermore, viruses such as Influenza are increasingly recognized as important etiologic agents in community acquired pneumonia. Within the U.S. alone, approximately 12.9 million people are heavy drinkers and chronic abuse of alcohol is known to increase the risk and severity of community acquired pneumonia. Given the lack of knowledge regarding Influenza disease in this population, we determined the effects of chronic alcohol consumption on Influenza virus infection. Herein, we report that mice exposed to chronic ethanol have sharp increases in morbidity, mortality, and pulmonary virus titers relative to controls. These increases in influenza severity correspond with inhibited pulmonary influenza-specific CD8 T cell responses. Further, chronic ethanol consumption results in an enhanced pulmonary lesion severity, similar to that recently described for pandemic influenzas. Together, our results suggest that chronic alcohol consumption may increase the risk for severe influenza virus infections by altering the pulmonary inflammatory environment and CD8 T cell response.
DOI: 10.4049/jimmunol.181.1.641
PubMed: 18566431
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Furthermore, viruses such as Influenza are increasingly recognized as important etiologic agents in community acquired pneumonia. Within the U.S. alone, approximately 12.9 million people are heavy drinkers and chronic abuse of alcohol is known to increase the risk and severity of community acquired pneumonia. Given the lack of knowledge regarding Influenza disease in this population, we determined the effects of chronic alcohol consumption on Influenza virus infection. Herein, we report that mice exposed to chronic ethanol have sharp increases in morbidity, mortality, and pulmonary virus titers relative to controls. These increases in influenza severity correspond with inhibited pulmonary influenza-specific CD8 T cell responses. Further, chronic ethanol consumption results in an enhanced pulmonary lesion severity, similar to that recently described for pandemic influenzas. Together, our results suggest that chronic alcohol consumption may increase the risk for severe influenza virus infections by altering the pulmonary inflammatory environment and CD8 T cell response.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">18566431</PMID><DateCompleted><Year>2008</Year><Month>07</Month><Day>28</Day></DateCompleted><DateRevised><Year>2019</Year><Month>05</Month><Day>16</Day></DateRevised><Article PubModel="Print"><Journal><ISSN IssnType="Print">0022-1767</ISSN><JournalIssue CitedMedium="Print"><Volume>181</Volume><Issue>1</Issue><PubDate><Year>2008</Year><Month>Jul</Month><Day>01</Day></PubDate></JournalIssue><Title>Journal of immunology (Baltimore, Md. : 1950)</Title><ISOAbbreviation>J. Immunol.</ISOAbbreviation></Journal><ArticleTitle>Chronic alcohol consumption increases the severity of murine influenza virus infections.</ArticleTitle><Pagination><MedlinePgn>641-8</MedlinePgn></Pagination><Abstract><AbstractText>Respiratory infections with both seasonal as well as potential pandemic Influenza viruses represent a significant burden on human health. Furthermore, viruses such as Influenza are increasingly recognized as important etiologic agents in community acquired pneumonia. Within the U.S. alone, approximately 12.9 million people are heavy drinkers and chronic abuse of alcohol is known to increase the risk and severity of community acquired pneumonia. Given the lack of knowledge regarding Influenza disease in this population, we determined the effects of chronic alcohol consumption on Influenza virus infection. Herein, we report that mice exposed to chronic ethanol have sharp increases in morbidity, mortality, and pulmonary virus titers relative to controls. These increases in influenza severity correspond with inhibited pulmonary influenza-specific CD8 T cell responses. Further, chronic ethanol consumption results in an enhanced pulmonary lesion severity, similar to that recently described for pandemic influenzas. Together, our results suggest that chronic alcohol consumption may increase the risk for severe influenza virus infections by altering the pulmonary inflammatory environment and CD8 T cell response.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Meyerholz</LastName><ForeName>David K</ForeName><Initials>DK</Initials><AffiliationInfo><Affiliation>Department of Pathology, University of Iowa, Iowa City, IA 52242, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Edsen-Moore</LastName><ForeName>Michelle</ForeName><Initials>M</Initials></Author><Author ValidYN="Y"><LastName>McGill</LastName><ForeName>Jodi</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>Coleman</LastName><ForeName>Ruth A</ForeName><Initials>RA</Initials></Author><Author ValidYN="Y"><LastName>Cook</LastName><ForeName>Robert T</ForeName><Initials>RT</Initials></Author><Author ValidYN="Y"><LastName>Legge</LastName><ForeName>Kevin L</ForeName><Initials>KL</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AA014405</GrantID><Acronym>AA</Acronym><Agency>NIAAA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 AA014405-05</GrantID><Acronym>AA</Acronym><Agency>NIAAA NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>AA-014405</GrantID><Acronym>AA</Acronym><Agency>NIAAA NIH HHS</Agency><Country>United States</Country></Grant></GrantList><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType><PublicationType UI="D052061">Research Support, N.I.H., Extramural</PublicationType><PublicationType UI="D013485">Research Support, Non-U.S. Gov't</PublicationType></PublicationTypeList></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>J 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