Exposure to combustion generated environmentally persistent free radicals enhances severity of influenza virus infection.
Identifieur interne : 000448 ( PubMed/Corpus ); précédent : 000447; suivant : 000449Exposure to combustion generated environmentally persistent free radicals enhances severity of influenza virus infection.
Auteurs : Greg I. Lee ; Jordy Saravia ; Dahui You ; Bishwas Shrestha ; Sridhar Jaligama ; Valerie Y. Hebert ; Tammy R. Dugas ; Stephania A. CormierSource :
- Particle and fibre toxicology [ 1743-8977 ] ; 2014.
English descriptors
- KwdEn :
- Adaptive Immunity (drug effects), Animals, Animals, Newborn, Dinoprost (analogs & derivatives), Dinoprost (metabolism), Free Radicals (toxicity), Glutathione (metabolism), Humans, Influenza A Virus, H1N1 Subtype (immunology), Influenza A Virus, H1N1 Subtype (pathogenicity), Inhalation Exposure (adverse effects), Lung (drug effects), Lung (immunology), Lung (physiopathology), Lung (virology), Mice, Mice, Inbred C57BL, Mice, Transgenic, Orthomyxoviridae Infections (chemically induced), Orthomyxoviridae Infections (immunology), Orthomyxoviridae Infections (physiopathology), Orthomyxoviridae Infections (virology), Oxidative Stress (drug effects), Particulate Matter (toxicity), Risk Assessment, Superoxide Dismutase (genetics), Superoxide Dismutase (metabolism), T-Lymphocytes, Regulatory (drug effects), T-Lymphocytes, Regulatory (immunology), T-Lymphocytes, Regulatory (virology), Time Factors, Viral Load.
- MESH :
- chemical , analogs & derivatives : Dinoprost.
- adverse effects : Inhalation Exposure.
- chemically induced : Orthomyxoviridae Infections.
- drug effects : Adaptive Immunity, Lung, Oxidative Stress, T-Lymphocytes, Regulatory.
- chemical , genetics : Superoxide Dismutase.
- immunology : Influenza A Virus, H1N1 Subtype, Lung, Orthomyxoviridae Infections, T-Lymphocytes, Regulatory.
- chemical , metabolism : Dinoprost, Glutathione, Superoxide Dismutase.
- pathogenicity : Influenza A Virus, H1N1 Subtype.
- physiopathology : Lung, Orthomyxoviridae Infections.
- chemical , toxicity : Free Radicals, Particulate Matter.
- virology : Lung, Orthomyxoviridae Infections, T-Lymphocytes, Regulatory.
- Animals, Animals, Newborn, Humans, Mice, Mice, Inbred C57BL, Mice, Transgenic, Risk Assessment, Time Factors, Viral Load.
Abstract
Exposures to elevated levels of particulate matter (PM) enhance severity of influenza virus infection in infants. The biological mechanism responsible for this phenomenon is unknown. The recent identification of environmentally persistent free radicals (EPFRs) associated with PM from a variety of combustion sources suggests its role in the enhancement of influenza disease severity.
DOI: 10.1186/s12989-014-0057-1
PubMed: 25358535
Links to Exploration step
pubmed:25358535Le document en format XML
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Lee</name></author><author><name sortKey="Saravia, Jordy" sort="Saravia, Jordy" uniqKey="Saravia J" first="Jordy" last="Saravia">Jordy Saravia</name></author><author><name sortKey="You, Dahui" sort="You, Dahui" uniqKey="You D" first="Dahui" last="You">Dahui You</name></author><author><name sortKey="Shrestha, Bishwas" sort="Shrestha, Bishwas" uniqKey="Shrestha B" first="Bishwas" last="Shrestha">Bishwas Shrestha</name></author><author><name sortKey="Jaligama, Sridhar" sort="Jaligama, Sridhar" uniqKey="Jaligama S" first="Sridhar" last="Jaligama">Sridhar Jaligama</name></author><author><name sortKey="Hebert, Valerie Y" sort="Hebert, Valerie Y" uniqKey="Hebert V" first="Valerie Y" last="Hebert">Valerie Y. Hebert</name></author><author><name sortKey="Dugas, Tammy R" sort="Dugas, Tammy R" uniqKey="Dugas T" first="Tammy R" last="Dugas">Tammy R. Dugas</name></author><author><name sortKey="Cormier, Stephania A" sort="Cormier, Stephania A" uniqKey="Cormier S" first="Stephania A" last="Cormier">Stephania A. Cormier</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2014">2014</date><idno type="RBID">pubmed:25358535</idno><idno type="pmid">25358535</idno><idno type="doi">10.1186/s12989-014-0057-1</idno><idno type="wicri:Area/PubMed/Corpus">000448</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">000448</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Exposure to combustion generated environmentally persistent free radicals enhances severity of influenza virus infection.</title><author><name sortKey="Lee, Greg I" sort="Lee, Greg I" uniqKey="Lee G" first="Greg I" last="Lee">Greg I. Lee</name></author><author><name sortKey="Saravia, Jordy" sort="Saravia, Jordy" uniqKey="Saravia J" first="Jordy" last="Saravia">Jordy Saravia</name></author><author><name sortKey="You, Dahui" sort="You, Dahui" uniqKey="You D" first="Dahui" last="You">Dahui You</name></author><author><name sortKey="Shrestha, Bishwas" sort="Shrestha, Bishwas" uniqKey="Shrestha B" first="Bishwas" last="Shrestha">Bishwas Shrestha</name></author><author><name sortKey="Jaligama, Sridhar" sort="Jaligama, Sridhar" uniqKey="Jaligama S" first="Sridhar" last="Jaligama">Sridhar Jaligama</name></author><author><name sortKey="Hebert, Valerie Y" sort="Hebert, Valerie Y" uniqKey="Hebert V" first="Valerie Y" last="Hebert">Valerie Y. Hebert</name></author><author><name sortKey="Dugas, Tammy R" sort="Dugas, Tammy R" uniqKey="Dugas T" first="Tammy R" last="Dugas">Tammy R. Dugas</name></author><author><name sortKey="Cormier, Stephania A" sort="Cormier, Stephania A" uniqKey="Cormier S" first="Stephania A" last="Cormier">Stephania A. Cormier</name></author></analytic><series><title level="j">Particle and fibre toxicology</title><idno type="eISSN">1743-8977</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adaptive Immunity (drug effects)</term><term>Animals</term><term>Animals, Newborn</term><term>Dinoprost (analogs & derivatives)</term><term>Dinoprost (metabolism)</term><term>Free Radicals (toxicity)</term><term>Glutathione (metabolism)</term><term>Humans</term><term>Influenza A Virus, H1N1 Subtype (immunology)</term><term>Influenza A Virus, H1N1 Subtype (pathogenicity)</term><term>Inhalation Exposure (adverse effects)</term><term>Lung (drug effects)</term><term>Lung (immunology)</term><term>Lung (physiopathology)</term><term>Lung (virology)</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Orthomyxoviridae Infections (chemically induced)</term><term>Orthomyxoviridae Infections (immunology)</term><term>Orthomyxoviridae Infections (physiopathology)</term><term>Orthomyxoviridae Infections (virology)</term><term>Oxidative Stress (drug effects)</term><term>Particulate Matter (toxicity)</term><term>Risk Assessment</term><term>Superoxide Dismutase (genetics)</term><term>Superoxide Dismutase (metabolism)</term><term>T-Lymphocytes, Regulatory (drug effects)</term><term>T-Lymphocytes, Regulatory (immunology)</term><term>T-Lymphocytes, Regulatory (virology)</term><term>Time Factors</term><term>Viral Load</term></keywords><keywords scheme="MESH" type="chemical" qualifier="analogs & derivatives" xml:lang="en"><term>Dinoprost</term></keywords><keywords scheme="MESH" qualifier="adverse effects" xml:lang="en"><term>Inhalation Exposure</term></keywords><keywords scheme="MESH" qualifier="chemically induced" xml:lang="en"><term>Orthomyxoviridae Infections</term></keywords><keywords scheme="MESH" qualifier="drug effects" xml:lang="en"><term>Adaptive Immunity</term><term>Lung</term><term>Oxidative Stress</term><term>T-Lymphocytes, Regulatory</term></keywords><keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en"><term>Superoxide Dismutase</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term><term>Lung</term><term>Orthomyxoviridae Infections</term><term>T-Lymphocytes, Regulatory</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Dinoprost</term><term>Glutathione</term><term>Superoxide Dismutase</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Influenza A Virus, H1N1 Subtype</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Lung</term><term>Orthomyxoviridae Infections</term></keywords><keywords scheme="MESH" type="chemical" qualifier="toxicity" xml:lang="en"><term>Free Radicals</term><term>Particulate Matter</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Lung</term><term>Orthomyxoviridae Infections</term><term>T-Lymphocytes, Regulatory</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Animals, Newborn</term><term>Humans</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>Mice, Transgenic</term><term>Risk Assessment</term><term>Time Factors</term><term>Viral Load</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Exposures to elevated levels of particulate matter (PM) enhance severity of influenza virus infection in infants. The biological mechanism responsible for this phenomenon is unknown. The recent identification of environmentally persistent free radicals (EPFRs) associated with PM from a variety of combustion sources suggests its role in the enhancement of influenza disease severity.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">25358535</PMID><DateCompleted><Year>2015</Year><Month>03</Month><Day>30</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic"><Journal><ISSN IssnType="Electronic">1743-8977</ISSN><JournalIssue CitedMedium="Internet"><Volume>11</Volume><PubDate><Year>2014</Year><Month>Oct</Month><Day>30</Day></PubDate></JournalIssue><Title>Particle and fibre toxicology</Title><ISOAbbreviation>Part Fibre Toxicol</ISOAbbreviation></Journal><ArticleTitle>Exposure to combustion generated environmentally persistent free radicals enhances severity of influenza virus infection.</ArticleTitle><Pagination><MedlinePgn>57</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1186/s12989-014-0057-1</ELocationID><Abstract><AbstractText Label="BACKGROUND" NlmCategory="BACKGROUND">Exposures to elevated levels of particulate matter (PM) enhance severity of influenza virus infection in infants. The biological mechanism responsible for this phenomenon is unknown. The recent identification of environmentally persistent free radicals (EPFRs) associated with PM from a variety of combustion sources suggests its role in the enhancement of influenza disease severity.</AbstractText><AbstractText Label="METHODS" NlmCategory="METHODS">Neonatal mice (< seven days of age) were exposed to DCB230 (combustion derived PM with a chemisorbed EPFR), DCB50 (non-EPFR PM sample), or air for 30 minutes/day for seven consecutive days. Four days post-exposure, neonates were infected with influenza intranasally at 1.25 TCID50/neonate. Neonates were assessed for morbidity (% weight gain, peak pulmonary viral load, and viral clearance) and percent survival. Lungs were isolated and assessed for oxidative stress (8-isoprostanes and glutathione levels), adaptive immune response to influenza, and regulatory T cells (Tregs). The role of the EPFR was also assessed by use of transgenic mice expressing human superoxide dismutase 2.</AbstractText><AbstractText Label="RESULTS" NlmCategory="RESULTS">Neonates exposed to EPFRs had significantly enhanced morbidity and decreased survival following influenza infection. Increased oxidative stress was also observed in EPFR exposed neonates. This correlated with increased pulmonary Tregs and dampened protective T cell responses to influenza infection. Reduction of EPFR-induced oxidative stress attenuated these effects.</AbstractText><AbstractText Label="CONCLUSIONS" NlmCategory="CONCLUSIONS">Neonatal exposure to EPFR containing PM resulted in pulmonary oxidative stress and enhanced influenza disease severity. EPFR-induced oxidative stress resulted in increased presence of Tregs in the lungs and subsequent suppression of adaptive immune response to influenza.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Lee</LastName><ForeName>Greg I</ForeName><Initials>GI</Initials></Author><Author ValidYN="Y"><LastName>Saravia</LastName><ForeName>Jordy</ForeName><Initials>J</Initials></Author><Author ValidYN="Y"><LastName>You</LastName><ForeName>Dahui</ForeName><Initials>D</Initials></Author><Author ValidYN="Y"><LastName>Shrestha</LastName><ForeName>Bishwas</ForeName><Initials>B</Initials></Author><Author ValidYN="Y"><LastName>Jaligama</LastName><ForeName>Sridhar</ForeName><Initials>S</Initials></Author><Author ValidYN="Y"><LastName>Hebert</LastName><ForeName>Valerie Y</ForeName><Initials>VY</Initials></Author><Author ValidYN="Y"><LastName>Dugas</LastName><ForeName>Tammy R</ForeName><Initials>TR</Initials></Author><Author ValidYN="Y"><LastName>Cormier</LastName><ForeName>Stephania A</ForeName><Initials>SA</Initials></Author></AuthorList><Language>eng</Language><GrantList CompleteYN="Y"><Grant><GrantID>R01 AI090059</GrantID><Acronym>AI</Acronym><Agency>NIAID NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01ES015050</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P42 ES013648</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>P42ES013648</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01 ES015050</GrantID><Acronym>ES</Acronym><Agency>NIEHS NIH HHS</Agency><Country>United States</Country></Grant><Grant><GrantID>R01AI090059</GrantID><Acronym>AI</Acronym><Agency>NIAID 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><ArticleDate DateType="Electronic"><Year>2014</Year><Month>10</Month><Day>30</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Part Fibre Toxicol</MedlineTA><NlmUniqueID>101236354</NlmUniqueID><ISSNLinking>1743-8977</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005609">Free Radicals</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D052638">Particulate Matter</NameOfSubstance></Chemical><Chemical><RegistryNumber>27415-26-5</RegistryNumber><NameOfSubstance UI="C075750">8-epi-prostaglandin F2alpha</NameOfSubstance></Chemical><Chemical><RegistryNumber>B7IN85G1HY</RegistryNumber><NameOfSubstance UI="D015237">Dinoprost</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber><NameOfSubstance UI="D013482">Superoxide Dismutase</NameOfSubstance></Chemical><Chemical><RegistryNumber>EC 1.15.1.1</RegistryNumber><NameOfSubstance UI="C431683">superoxide dismutase 2</NameOfSubstance></Chemical><Chemical><RegistryNumber>GAN16C9B8O</RegistryNumber><NameOfSubstance UI="D005978">Glutathione</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D056704" MajorTopicYN="N">Adaptive Immunity</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D000831" MajorTopicYN="N">Animals, Newborn</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D015237" MajorTopicYN="N">Dinoprost</DescriptorName><QualifierName UI="Q000031" MajorTopicYN="N">analogs & derivatives</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005609" MajorTopicYN="N">Free Radicals</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005978" MajorTopicYN="N">Glutathione</DescriptorName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D053118" MajorTopicYN="N">Influenza A Virus, H1N1 Subtype</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000472" MajorTopicYN="Y">pathogenicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D019570" MajorTopicYN="N">Inhalation Exposure</DescriptorName><QualifierName UI="Q000009" MajorTopicYN="N">adverse effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D008168" MajorTopicYN="N">Lung</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="Y">drug effects</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008822" MajorTopicYN="N">Mice, Transgenic</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009976" MajorTopicYN="N">Orthomyxoviridae Infections</DescriptorName><QualifierName UI="Q000139" MajorTopicYN="Y">chemically induced</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName><QualifierName UI="Q000821" MajorTopicYN="Y">virology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018384" MajorTopicYN="N">Oxidative Stress</DescriptorName><QualifierName UI="Q000187" MajorTopicYN="N">drug effects</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D052638" MajorTopicYN="N">Particulate Matter</DescriptorName><QualifierName UI="Q000633" MajorTopicYN="Y">toxicity</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D018570" MajorTopicYN="N">Risk Assessment</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D013482" MajorTopicYN="N">Superoxide Dismutase</DescriptorName><QualifierName UI="Q000235" MajorTopicYN="N">genetics</QualifierName><QualifierName UI="Q000378" MajorTopicYN="N">metabolism</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D050378" MajorTopicYN="N">T-Lymphocytes, 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