Integrated Signals Between IL-13, IL-4, and IL-5 Regulate Airways Hyperreactivity

DOI PDF 被引用文献6件
  • Dianne C Webb
    Division of Biochemistry and Molecular Biology, The John Curtin School of Medical Research, Australian National University , Canberra ,
  • Andrew N J McKenzie
    Medical Research Council Laboratory of Molecular Biology , Cambridge ,
  • Aulikki M L Koskinen
    Division of Biochemistry and Molecular Biology, The John Curtin School of Medical Research, Australian National University , Canberra ,
  • Ming Yang
    Division of Biochemistry and Molecular Biology, The John Curtin School of Medical Research, Australian National University , Canberra ,
  • Joërg Mattes
    Division of Biochemistry and Molecular Biology, The John Curtin School of Medical Research, Australian National University , Canberra ,
  • Paul S Foster
    Division of Biochemistry and Molecular Biology, The John Curtin School of Medical Research, Australian National University , Canberra ,

書誌事項

公開日
2000-07-01
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.165.1.108
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>In this investigation, we have examined the integrated relationship between IL-13, IL-4, and IL-5 for the development of airways hyperreactivity (AHR) in a model of asthma in BALB/c mice. Sensitization and aeroallergen challenge of both wild-type (WT) and IL-13 gene-targeted (IL-13−/−) mice induced allergic disease that was characterized by pulmonary eosinophilia and AHR to β-methacholine. Although these responses in IL-13−/− mice were heightened compared with WT, they could be reduced to the level in nonallergic mice by the concomitant neutralization of IL-4. Mice in which both IL-4 and IL-13 were depleted displayed a marked reduction in tissue eosinophils, despite the development of a blood eosinophilia. Similar neutralization of IL-4 in WT mice only partially reduced AHR with no effect on tissue eosinophilia. In addition, neutralization of IL-5 in IL-13−/− mice, but not in WT mice, inhibited AHR, suggesting that tissue eosinophilia is linked to the mechanism underlying AHR only in the absence of IL-13. Additionally, mucus hypersecretion was attenuated in IL-13−/− mice, despite the persistence of AHR. Taken together, our data suggest both a modulatory role for IL-13 during sensitization and a proinflammatory role during aeroallergen challenge. The latter process appears redundant with respect to IL-4.</jats:p>

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