Potential Role for Alternatively Activated Macrophages in the Secondary Bacterial Infection During Recovery from Influenza
Identifieur interne : 000C20 ( Main/Exploration ); précédent : 000C19; suivant : 000C21Potential Role for Alternatively Activated Macrophages in the Secondary Bacterial Infection During Recovery from Influenza
Auteurs : Wilbur H. Chen [États-Unis] ; Franklin R. Toapanta [États-Unis] ; Kari Ann Shirey [États-Unis] ; Lei Zhang [États-Unis] ; Angeliki Giannelou [États-Unis] ; Carly Page [États-Unis] ; Matthew B. Frieman [États-Unis] ; Stefanie Vogel [États-Unis] ; Alan S. Cross [États-Unis]Source :
- Immunology letters [ 0165-2478 ] ; 2011.
Abstract
Secondary bacterial infections are a common complication of influenza. Innate immune host defenses appear to be impaired following influenza, leading to susceptibility to subsequent bacterial infections. Alternatively activated macrophages (AAM) in the lungs may play a critical role in eliciting the hypersusceptibility to secondary bacterial pneumonia.
C57BL6 mice were challenged with sublethal doses of the mouse-adapted A/PR/8/34 (PR8) influenza virus or saline and allowed to recover. At complete recovery (day 14), mice were re-challenged with sublethal doses of
PR8-recovered mice developed a rapidly fatal pulmonary infection to a 100-fold sublethal pneumococcal challenge, whereas PR8-naive mice demonstrated no mortality or illness. The cytokines which induce AAM (IL-4 and IL-13) and the expression of genes associated with AAM (Arginase-1, FIZZ1, and YM1) were elevated after PR8 infection. Flow cytometry suggests that alveolar macrophages demonstrate the AAM-phenotype, as indicated by MGL-1 and MHCII expression, in response to PR8 infection. Recovery from PR8 was associated with blunted cytokine responses to TLR ligands.
The mechanisms of immune regulation during recovery from influenza are being elucidated. We provide evidence that pulmonary AAM are induced during influenza infection and may contribute to the elicitation of hypersusceptibility to a secondary bacterial infection.
Url:
DOI: 10.1016/j.imlet.2011.10.009
PubMed: 22037624
PubMed Central: 3243824
Affiliations:
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Chen</name><affiliation wicri:level="2"><nlm:aff id="A1">Center for Vaccine Development, University of Maryland School of Medicine, Baltimore, MD</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Center for Vaccine Development, University of Maryland School of Medicine, Baltimore</wicri:cityArea></affiliation></author><author><name sortKey="Toapanta, Franklin R" sort="Toapanta, Franklin R" uniqKey="Toapanta F" first="Franklin R." last="Toapanta">Franklin R. Toapanta</name><affiliation wicri:level="2"><nlm:aff id="A1">Center for Vaccine Development, University of Maryland School of Medicine, Baltimore, MD</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Center for Vaccine Development, University of Maryland School of Medicine, Baltimore</wicri:cityArea></affiliation></author><author><name sortKey="Shirey, Kari Ann" sort="Shirey, Kari Ann" uniqKey="Shirey K" first="Kari Ann" last="Shirey">Kari Ann Shirey</name><affiliation wicri:level="2"><nlm:aff id="A2">Department of Microbiology & Immunology, University of Maryland School of Medicine, Baltimore, MD</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Department of Microbiology & Immunology, University of Maryland School of Medicine, Baltimore</wicri:cityArea></affiliation></author><author><name sortKey="Zhang, Lei" sort="Zhang, Lei" uniqKey="Zhang L" first="Lei" last="Zhang">Lei Zhang</name><affiliation wicri:level="2"><nlm:aff id="A1">Center for Vaccine Development, University of Maryland School of Medicine, Baltimore, MD</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Center for Vaccine Development, University of Maryland School of Medicine, Baltimore</wicri:cityArea></affiliation></author><author><name sortKey="Giannelou, Angeliki" sort="Giannelou, Angeliki" uniqKey="Giannelou A" first="Angeliki" last="Giannelou">Angeliki Giannelou</name><affiliation wicri:level="2"><nlm:aff id="A1">Center for Vaccine Development, University of Maryland School of Medicine, Baltimore, MD</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Center for Vaccine Development, University of Maryland School of Medicine, Baltimore</wicri:cityArea></affiliation></author><author><name sortKey="Page, Carly" sort="Page, Carly" uniqKey="Page C" first="Carly" last="Page">Carly Page</name><affiliation wicri:level="2"><nlm:aff id="A2">Department of Microbiology & Immunology, University of Maryland School of Medicine, Baltimore, MD</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Department of Microbiology & Immunology, University of Maryland School of Medicine, Baltimore</wicri:cityArea></affiliation></author><author><name sortKey="Frieman, Matthew B" sort="Frieman, Matthew B" uniqKey="Frieman M" first="Matthew B." last="Frieman">Matthew B. Frieman</name><affiliation wicri:level="2"><nlm:aff id="A2">Department of Microbiology & Immunology, University of Maryland School of Medicine, Baltimore, MD</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Department of Microbiology & Immunology, University of Maryland School of Medicine, Baltimore</wicri:cityArea></affiliation></author><author><name sortKey="Vogel, Stefanie" sort="Vogel, Stefanie" uniqKey="Vogel S" first="Stefanie" last="Vogel">Stefanie Vogel</name><affiliation wicri:level="2"><nlm:aff id="A2">Department of Microbiology & Immunology, University of Maryland School of Medicine, Baltimore, MD</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Department of Microbiology & Immunology, University of Maryland School of Medicine, Baltimore</wicri:cityArea></affiliation></author><author><name sortKey="Cross, Alan S" sort="Cross, Alan S" uniqKey="Cross A" first="Alan S." last="Cross">Alan S. Cross</name><affiliation wicri:level="2"><nlm:aff id="A1">Center for Vaccine Development, University of Maryland School of Medicine, Baltimore, MD</nlm:aff><country xml:lang="fr">États-Unis</country><placeName><region type="state">Maryland</region></placeName><wicri:cityArea>Center for Vaccine Development, University of Maryland School of Medicine, Baltimore</wicri:cityArea></affiliation></author></analytic><series><title level="j">Immunology letters</title><idno type="ISSN">0165-2478</idno><idno type="eISSN">1879-0542</idno><imprint><date when="2011">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec id="S1"><title>Purpose</title><p id="P2">Secondary bacterial infections are a common complication of influenza. Innate immune host defenses appear to be impaired following influenza, leading to susceptibility to subsequent bacterial infections. Alternatively activated macrophages (AAM) in the lungs may play a critical role in eliciting the hypersusceptibility to secondary bacterial pneumonia.</p></sec><sec sec-type="methods" id="S2"><title>Methods</title><p id="P3">C57BL6 mice were challenged with sublethal doses of the mouse-adapted A/PR/8/34 (PR8) influenza virus or saline and allowed to recover. At complete recovery (day 14), mice were re-challenged with sublethal doses of <italic>Streptococcus pneumoniae</italic> serotype 3 (Sp3).</p></sec><sec id="S3"><title>Results</title><p id="P4">PR8-recovered mice developed a rapidly fatal pulmonary infection to a 100-fold sublethal pneumococcal challenge, whereas PR8-naive mice demonstrated no mortality or illness. The cytokines which induce AAM (IL-4 and IL-13) and the expression of genes associated with AAM (Arginase-1, FIZZ1, and YM1) were elevated after PR8 infection. Flow cytometry suggests that alveolar macrophages demonstrate the AAM-phenotype, as indicated by MGL-1 and MHCII expression, in response to PR8 infection. Recovery from PR8 was associated with blunted cytokine responses to TLR ligands.</p></sec><sec id="S4"><title>Conclusions</title><p id="P5">The mechanisms of immune regulation during recovery from influenza are being elucidated. We provide evidence that pulmonary AAM are induced during influenza infection and may contribute to the elicitation of hypersusceptibility to a secondary bacterial infection.</p></sec></div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Maryland</li></region></list><tree><country name="États-Unis"><region name="Maryland"><name sortKey="Chen, Wilbur H" sort="Chen, Wilbur H" uniqKey="Chen W" first="Wilbur H." last="Chen">Wilbur H. Chen</name></region><name sortKey="Cross, Alan S" sort="Cross, Alan S" uniqKey="Cross A" first="Alan S." last="Cross">Alan S. Cross</name><name sortKey="Frieman, Matthew B" sort="Frieman, Matthew B" uniqKey="Frieman M" first="Matthew B." last="Frieman">Matthew B. Frieman</name><name sortKey="Giannelou, Angeliki" sort="Giannelou, Angeliki" uniqKey="Giannelou A" first="Angeliki" last="Giannelou">Angeliki Giannelou</name><name sortKey="Page, Carly" sort="Page, Carly" uniqKey="Page C" first="Carly" last="Page">Carly Page</name><name sortKey="Shirey, Kari Ann" sort="Shirey, Kari Ann" uniqKey="Shirey K" first="Kari Ann" last="Shirey">Kari Ann Shirey</name><name sortKey="Toapanta, Franklin R" sort="Toapanta, Franklin R" uniqKey="Toapanta F" first="Franklin R." last="Toapanta">Franklin R. Toapanta</name><name sortKey="Vogel, Stefanie" sort="Vogel, Stefanie" uniqKey="Vogel S" first="Stefanie" last="Vogel">Stefanie Vogel</name><name sortKey="Zhang, Lei" sort="Zhang, Lei" uniqKey="Zhang L" first="Lei" last="Zhang">Lei Zhang</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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