Bronchial epithelial cells of atopic patients with asthma lack the ability to inactivate allergens.
The cause of asthma is still unknown. Though most asthmatic patients are atopic, only certain atopic subjects develop this disease, and atopic asthmatics recover from asthma after transplantation of lungs from nonasthmatic donors. Thus, there might be a primary local defect in the bronchial wall which affects the expression of asthma in atopic individuals. We show here that the bronchial epithelial cells from atopic patients with asthma are aberrantly permeable to the airborne allergen most often implicated in the pathogenesis of this disease, indicating how it can have access to the antigen-presenting cells (dendritic cells) below the apical surface of the epithelium in vivo. In addition, allergen exposure induces asthmatic epithelial cells to express granulocyte/macrophage colony-stimulating factor, a cytokine involved in the proliferation and function of dendritic cells.
Mori
L
L
Institute of Experimental Medicine, Milano, Italy.
Kleimberg
J
J
Mancini
C
C
Bellini
A
A
Marini
M
M
Mattoli
S
S
D000485:Allergens / Q000378:metabolism*; D000818:Animals; D039741:Antigens, Dermatophagoides; D001249:Asthma / Q000378:metabolism*; D001980:Bronchi / Q000166:cytology / Q000378:metabolism*; D002478:Cells, Cultured; D003713:Dendritic Cells / Q000276:immunology; D004848:Epithelium / Q000378:metabolism; D015870:Gene Expression; D006023:Glycoproteins / Q000378:metabolism; D016178:Granulocyte-Macrophage Colony-Stimulating Factor / Q000235:genetics / Q000378:metabolism; D006801:Humans; D006967:Hypersensitivity / Q000378:metabolism*; D008925:Mites / Q000276:immunology; D010539:Permeability; D012333:RNA, Messenger / Q000235:genetics
D000485:Allergens; D039741:Antigens, Dermatophagoides; D006023:Glycoproteins; D012333:RNA, Messenger; D016178:Granulocyte-Macrophage Colony-Stimulating Factor