Selective Blockade of NF-κB Activity in Airway Immune Cells Inhibits the Effector Phase of Experimental Asthma

DOI PDF 被引用文献4件
  • Christophe Desmet
    Laboratoire de Physiologie, Université de Liège , Liège ,
  • Philippe Gosset
    Institut National de la Santé et de la Recherche Médicale, Unité 416, Institut Pasteur de Lille , Lille ,
  • Bernard Pajak
    Laboratoire de Physiologie Animale, Institut de Biologie et de Médecine Moléculaires, Université Libre de Bruxelles , Gosselies ,
  • Didier Cataldo
    Service de Pneumologie, and Chimie Médicale, Centre de Thérapie Cellulaire et Moléculaire, Université de Liège , Liège ,
  • Mohamed Bentires-Alj
    Institut National de la Santé et de la Recherche Médicale, Unité 416, Institut Pasteur de Lille , Lille ,
  • Pierre Lekeux
    Laboratoire de Physiologie, Université de Liège , Liège ,
  • Fabrice Bureau
    Laboratoire de Physiologie, Université de Liège , Liège ,

書誌事項

公開日
2004-11-01
権利情報
  • https://academic.oup.com/pages/standard-publication-reuse-rights
DOI
  • 10.4049/jimmunol.173.9.5766
公開者
Oxford University Press (OUP)

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<jats:title>Abstract</jats:title> <jats:p>Knockout mice studies have revealed that NF-κB plays a critical role in Th2 cell differentiation and is therefore required for induction of allergic airway inflammation. However, the questions of whether NF-κB also plays a role in the effector phase of airway allergy and whether inhibiting NF-κB could have therapeutic value in the treatment of established asthma remain unanswered. To address these issues, we have assessed in OVA-sensitized wild-type mice the effects of selectively antagonizing NF-κB activity in the lungs during OVA challenge. Intratracheal administration of NF-κB decoy oligodeoxynucleotides to OVA-sensitized mice led to efficient nuclear transfection of airway immune cells, but not constitutive lung cells and draining lymph node cells, associated with abrogation of NF-κB activity in the airways upon OVA provocation. NF-κB inhibition was associated with strong attenuation of allergic lung inflammation, airway hyperresponsiveness, and local production of mucus, IL-5, IL-13, and eotaxin. IL-4 and OVA-specific IgE and IgG1 production was not reduced. This study demonstrates for the first time that activation of NF-κB in local immune cells is critically involved in the effector phase of allergic airway disease and that specific NF-κB inhibition in the lungs has therapeutic potential in the control of pulmonary allergy.</jats:p>

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