Neutrophils Induce a Novel Chemokine Receptors Repertoire During Influenza Pneumonia.

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  • Additional Information
    • Source:
      Publisher: Frontiers Media SA Country of Publication: Switzerland NLM ID: 101585359 Publication Model: eCollection Cited Medium: Internet ISSN: 2235-2988 (Electronic) Linking ISSN: 22352988 NLM ISO Abbreviation: Front Cell Infect Microbiol Subsets: MEDLINE
    • Publication Information:
      Original Publication: Lausanne : Frontiers Media SA
    • Subject Terms:
      Neutrophils/*immunology ; Orthomyxoviridae/*immunology ; Orthomyxoviridae Infections/*immunology ; Pneumonia, Viral/*immunology ; Receptors, Chemokine/*biosynthesis; Animals ; Disease Models, Animal ; Flow Cytometry ; Mice ; Neutrophils/chemistry
    • Abstract:
      Exaggerated host innate immune responses have been implicated in severe influenza pneumonia. We have previously demonstrated that excessive neutrophils recruited during influenza infection drive pulmonary pathology through induction of neutrophil extracellular traps (NETs) and release of extracellular histones. Chemokine receptors (CRs) are essential in the recruitment and activation of leukocytes. Although neutrophils have been implicated in influenza pathogenesis, little is known about their phenotypic changes, including expression of CRs occurring in the infected -lung microenvironment. Here, we examined CC and CXC CRs detection in circulating as well as lung-recruited neutrophils during influenza infection in mice using flow cytometry analyses. Our studies revealed that lung-recruited neutrophils displayed induction of CRs, including CCR1, CCR2, CCR3, CCR5, CXCR1, CXCR3, and CXCR4, all of which were marginally induced in circulating neutrophils. CXCR2 was the most predominant CR observed in both circulating and lung-infiltrated neutrophils after infection. The stimulation of these induced CRs modulated neutrophil phagocytic activity, ligand-specific neutrophil migration, bacterial killing, and NETs induction ex vivo . These findings indicate that neutrophils induce a novel CR repertoire in the infectious lung microenvironment, which alters their functionality during influenza pneumonia.
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    • Grant Information:
      P20 GM103648 United States GM NIGMS NIH HHS
    • Contributed Indexing:
      Keywords: acute lung injury; chemokine receptor; influenza; mouse model; neutrophil
    • Accession Number:
      0 (Receptors, Chemokine)
    • Publication Date:
      Date Created: 20190502 Date Completed: 20191209 Latest Revision: 20200309
    • Publication Date:
      20240829
    • Accession Number:
      PMC6476945
    • Accession Number:
      10.3389/fcimb.2019.00108
    • Accession Number:
      31041196