IL-6 Is Required for Airway Mucus Production Induced by Inhaled Fungal Allergens

DOI PDF 被引用文献6件
  • Wendy A. Neveu
    *Department of Medicine, Division of Immunobiology, and
  • Jenna B. Allard
    †Department of Medicine, Division of Pulmonary Disease and Critical Care, University of Vermont, Burlington VT 05405; and
  • Oliver Dienz
    *Department of Medicine, Division of Immunobiology, and
  • Matthew J. Wargo
    †Department of Medicine, Division of Pulmonary Disease and Critical Care, University of Vermont, Burlington VT 05405; and
  • Gennaro Ciliberto
    ‡Istituto di Ricerche di Biologia Molecolare P. Angeletti, Roma, Italy
  • Laurie A. Whittaker
    †Department of Medicine, Division of Pulmonary Disease and Critical Care, University of Vermont, Burlington VT 05405; and
  • Mercedes Rincon
    *Department of Medicine, Division of Immunobiology, and

説明

<jats:title>Abstract</jats:title> <jats:p>Allergic asthma is caused by inhaled allergens and is characterized by airway eosinophilia, as well as mucus hypersecretion, which can lead to airflow obstruction. Despite the association of increased IL-6 levels with human atopic asthma, the contribution of IL-6 to the development of allergic airway inflammation triggered by inhaled allergens remains unclear. In this study, we examined the role of IL-6 in a mouse model of allergic airway inflammation induced by direct airway exposure to extracts of Aspergillus fumigatus, a common allergen in humans. We show that inhaled A. fumigatus extracts rapidly trigger the production of IL-6 in the airways. IL-6 appears to be dispensable for the recruitment of eosinophils to the lung during the development of allergic airway inflammation. However, IL-6 is essential for mucus hypersecretion by airway epithelial cells triggered in response to inhaled A. fumigatus Ags. Impaired mucus production caused by IL-6 deficiency correlates with a severe reduction in the levels of IL-13, a major inducer of mucin glycoproteins. Thus, IL-6 is a key regulator of specific hallmark features of allergic airway inflammation and it could be a potential target for pulmonary diseases that are associated with goblet cell metaplasia and mucus hypersecretion.</jats:p>

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