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Ozone-induced eosinophil recruitment to airways is altered by antigen sensitization and tumor necrosis factor- α blockade.

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  • معلومة اضافية
    • المصدر:
      Publisher: published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society Country of Publication: United States NLM ID: 101607800 Publication Model: Print Cited Medium: Internet ISSN: 2051-817X (Electronic) Linking ISSN: 2051817X NLM ISO Abbreviation: Physiol Rep Subsets: MEDLINE
    • بيانات النشر:
      Original Publication: [Malden MA] : published by Wiley Periodicals, Inc. on behalf of the American Physiological Society and The Physiological Society, 2013-
    • الموضوع:
    • نبذة مختصرة :
      Ozone is an atmospheric pollutant that causes lung inflammation and airway hyperresponsiveness. Ozone's effects occur in two distinct phases that are mediated by different populations of eosinophils. In the acute phase 1 day after exposure, mature airway-resident eosinophils alter parasympathetic nerve function that results in airway hyperresponsiveness. At this time point, the severity of hyperresponsiveness correlates with the number of eosinophils in close proximity to airway nerves, but not with eosinophils in bronchoalveolar lavage. Three days later, newly divided eosinophils are recruited to airways by a tumor necrosis factor- α -dependent mechanism. These new eosinophils paradoxically attenuate ozone-induced airway hyperresponsiveness. Ozone's effects on airway tissue eosinophils and nerve-associated eosinophils 3 days after exposure are unknown. Thus, we tested ozone's effects on eosinophils in airway subepithelium and around airway nerves 1 and 3 days after ozone in nonsensitized and ovalbumin-sensitized guinea pigs with or without the tumor necrosis factor- α antagonist, etanercept, and compared changes in eosinophils with ozone-induced airway hyperresponsiveness. More eosinophils were present in small, noncartilaginous airways and along small airway nerves compared to large cartilaginous airways in all treatment groups. The number of airway and nerve-associated eosinophils were unaffected 1 day after ozone exposure, whereas significantly fewer airway eosinophils were present 3 days later. Airway and nerve-associated eosinophils were also decreased in small airways 3 days after ozone in sensitized animals. These changes were blocked by etanercept. Airway eosinophils, but not nerve-associated or bronchoalveolar lavage eosinophils correlated with airway hyperresponsiveness 3 days after ozone. Our findings indicate ozone causes persistent alterations in airway eosinophils and reinforce the importance of characterizing eosinophils' effects within distinct airway compartments.
      (© 2017 The Authors. Physiological Reports published by Wiley Periodicals, Inc. on behalf of The Physiological Society and the American Physiological Society.)
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    • Grant Information:
      K08 HL121254 United States HL NHLBI NIH HHS; T32 HL083808 United States HL NHLBI NIH HHS; TL1 TR000129 United States TR NCATS NIH HHS
    • Contributed Indexing:
      Keywords: TNF α; Airway; asthma; eosinophil; nerve; ozone
    • الرقم المعرف:
      0 (Immunosuppressive Agents)
      0 (Tumor Necrosis Factor-alpha)
      66H7ZZK23N (Ozone)
      OP401G7OJC (Etanercept)
    • الموضوع:
      Date Created: 20171216 Date Completed: 20180718 Latest Revision: 20230812
    • الموضوع:
      20231215
    • الرقم المعرف:
      PMC5742702
    • الرقم المعرف:
      10.14814/phy2.13538
    • الرقم المعرف:
      29242307