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1000 Titel
  • Macrophage Polarization Modulated by Porcine Circovirus Type 2 Facilitates Bacterial Coinfection
1000 Autor/in
  1. Zhang, Wen |
  2. Fu, Zhendong |
  3. Yin, Hongyan |
  4. Han, Qingbing |
  5. Fan, Wenhui |
  6. Wang, Fangkun |
  7. Shang, Yingli |
1000 Erscheinungsjahr 2021
1000 Publikationstyp
  1. Artikel |
1000 Online veröffentlicht
  • 2021-07-28
1000 Erschienen in
1000 Quellenangabe
  • 12:688294
1000 Copyrightjahr
  • 2021
1000 Embargo
  • 2022-01-30
1000 Lizenz
1000 Verlagsversion
  • https://doi.org/10.3389/fimmu.2021.688294 |
  • https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8355693/ |
1000 Publikationsstatus
1000 Begutachtungsstatus
1000 Abstract/Summary
  • <jats:p>Polarization of macrophages to different functional states is important for mounting responses against pathogen infections. Macrophages are the major target cells of porcine circovirus type 2 (PCV2), which is the primary causative agent of porcine circovirus–associated disease (PCVAD) leading to immense economic losses in the global swine industry. Clinically, PCV2 is often found to increase risk of other pathogenic infections yet the underlying mechanisms remain to be elusive. Here we found that PCV2 infection skewed macrophages toward a M1 status through reprogramming expression of a subset of M1-associated genes and M2-associated genes. Mechanistically, induction of M1-associated genes by PCV2 infection is dependent on activation of nuclear factor kappa B (NF-κB) and c-jun N-terminal kinase (JNK) signaling pathways whereas suppression of M2-associated genes by PCV2 is <jats:italic>via</jats:italic> inhibiting expression of jumonji domain containing-3 (JMJD3), a histone 3 Lys27 (H3K27) demethylase that regulates M2 activation of macrophages. Finally, we identified that PCV2 capsid protein (Cap) directly inhibits <jats:italic>JMJD3</jats:italic> transcription to restrain expression of interferon regulatory factor (<jats:italic>IRF4</jats:italic>) that controls M2 macrophage polarization. Consequently, sustained infection of PCV2 facilitates bacterial infection <jats:italic>in vitro</jats:italic>. In summary, these findings showed that PCV2 infection functionally modulated M1 macrophage polarization <jats:italic>via</jats:italic> targeting canonical signals and epigenetic histone modification, which contributes to bacterial coinfection and virial pathogenesis.</jats:p>
1000 Sacherschließung
lokal Circoviridae Infections/immunology [MeSH]
lokal JNK Mitogen-Activated Protein Kinases/metabolism [MeSH]
lokal Salmonella Infections/metabolism [MeSH]
lokal Actinobacillus Infections/microbiology [MeSH]
lokal Mice, Inbred C57BL [MeSH]
lokal Circoviridae Infections/virology [MeSH]
lokal JMJD3
lokal Host-Pathogen Interactions [MeSH]
lokal Macrophages/metabolism [MeSH]
lokal Interferon Regulatory Factors/metabolism [MeSH]
lokal Myeloid Differentiation Factor 88/genetics [MeSH]
lokal Macrophages/immunology [MeSH]
lokal Myeloid Differentiation Factor 88/metabolism [MeSH]
lokal bacterial coinfection
lokal Actinobacillus Infections/immunology [MeSH]
lokal Cap
lokal Circovirus/immunology [MeSH]
lokal Phenotype [MeSH]
lokal Circovirus/pathogenicity [MeSH]
lokal Disease Models, Animal [MeSH]
lokal Chromatin Assembly and Disassembly [MeSH]
lokal Immunology
lokal Coinfection [MeSH]
lokal Macrophages/microbiology [MeSH]
lokal Macrophages/virology [MeSH]
lokal Actinobacillus Infections/metabolism [MeSH]
lokal Salmonella typhimurium/pathogenicity [MeSH]
lokal Animals [MeSH]
lokal Jumonji Domain-Containing Histone Demethylases/metabolism [MeSH]
lokal Salmonella Infections/microbiology [MeSH]
lokal Mice, Knockout [MeSH]
lokal Actinobacillus pleuropneumoniae/pathogenicity [MeSH]
lokal Epigenesis, Genetic [MeSH]
lokal Mice [MeSH]
lokal NF-kappa B/metabolism [MeSH]
lokal Actinobacillus pleuropneumoniae/immunology [MeSH]
lokal Salmonella Infections/immunology [MeSH]
lokal Salmonella typhimurium/immunology [MeSH]
lokal macrophage polarization
lokal Signal Transduction [MeSH]
lokal Cells, Cultured [MeSH]
lokal PCV2
1000 Liste der Beteiligten
  1. https://frl.publisso.de/adhoc/uri/WmhhbmcsIFdlbg==|https://frl.publisso.de/adhoc/uri/RnUsIFpoZW5kb25n|https://frl.publisso.de/adhoc/uri/WWluLCBIb25neWFu|https://frl.publisso.de/adhoc/uri/SGFuLCBRaW5nYmluZw==|https://frl.publisso.de/adhoc/uri/RmFuLCBXZW5odWk=|https://frl.publisso.de/adhoc/uri/V2FuZywgRmFuZ2t1bg==|https://frl.publisso.de/adhoc/uri/U2hhbmcsIFlpbmdsaQ==
1000 Hinweis
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1000 Erstellt am 2024-05-14T11:06:47.335+0200
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