Fungal allergen beta-glucans trigger p38 mitogen-activated protein kinase-mediated IL-6 translation in lung epithelial cells

UMMS Affiliation

Program in Molecular Medicine

Publication Date


Document Type



Allergens; Animals; Aspergillus fumigatus; Asthma; CD4-Positive T-Lymphocytes; Cells, Cultured; Epithelial Cells; Gene Expression Regulation; Interleukin-6; Lung; MAP Kinase Signaling System; Mice; Mice, Knockout; Respiratory Mucosa; beta-Glucans; p38 Mitogen-Activated Protein Kinases


Biochemistry | Cell Biology | Cellular and Molecular Physiology | Immunity | Molecular Biology


In addition to immune cells, airway epithelial cells can contribute to and shape the immune response in the lung by secreting specific cytokines. IL-6 is a key factor in determining the effector fate of CD4(+) T cells. Here we show that under basal conditions, the IL-6 gene is already highly expressed in lung epithelial cells, but not in immune cells resident in the lung. However, upon exposure of the lungs to fungal allergens, the direct contact of beta-glucans present in the fungus cell wall with lung epithelial cells is sufficient to trigger the rapid synthesis and secretion of IL-6 protein. This posttranscriptional regulation of IL-6 in response to fungal extracts is mediated by the p38 mitogen-activated protein kinase pathway. The inhalation of beta-glucans with a nonallergenic antigen is sufficient to provide an adjuvant effect that leads to mucous hyperplasia in the airways. Thus, beta-glucans may constitute a common determinant of the fungal and plant-derived allergens responsible for some of the pathological features in allergic asthma.

DOI of Published Version



Am J Respir Cell Mol Biol. 2011 Dec;45(6):1133-41. doi: 10.1165/rcmb.2011-0054OC. Epub 2011 Jun 3. Link to article on publisher's site

Journal/Book/Conference Title

American journal of respiratory cell and molecular biology

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Link to Article in PubMed

PubMed ID