Loss of caveolin-1 from bronchial epithelial cells and monocytes in human subjects with asthma

• Published in: Allergy (Copenhagen) Vol. 67; no. 12; pp. 1601 - 1604
• Main Authors: Bains, S. N., Tourkina, E., Atkinson, C., Joseph, K., Tholanikunnel, B., Chu, H. W., Riemer, E. C., Martin, R., Hoffman, S.
• Format: Journal Article
• Language: English
• Published: Oxford Blackwell Publishing Ltd 01.12.2012; Blackwell
• Subjects: allergen; Animal models; Animals; Aspergillus fumigatus; Asthma; Asthma - metabolism; Biological and medical sciences; Biopsy; Bronchi - metabolism; Caveolin 1 - deficiency; Caveolin 1 - metabolism; caveolin-1; Cellular biology; Chronic obstructive pulmonary disease, asthma; Collagen (type I); Dermatology; Disease Models, Animal; Epithelial cells; Epithelial Cells - metabolism; epithelium; Extracellular matrix; Extracellular Matrix Proteins - metabolism; Female; Fibrosis; Fundamental and applied biological sciences. Psychology; Fundamental immunology; Gene expression; Humans; Immunohistochemistry; Inflammation; Lung; Lung - metabolism; Lung - pathology; Medical sciences; Mice; Monocytes; Monocytes - metabolism; Peripheral blood; Pneumology; Proteins; regulatory proteins; Sarcoidosis. Granulomatous diseases of unproved etiology. Connective tissue diseases. Elastic tissue diseases. Vasculitis; Signal Transduction; Tenascin; Human; Lung disease; Allergy; Immunopathology; Monocyte; Respiratory disease; Dermatology; Bronchus; Epithelium; Respiratory system; Asthma; Respiratory tract; Caveolin 1; Immunology; Bronchus disease; Epithelial cell; Obstructive pulmonary disease; Allergen
• ISSN: 0105-4538; 1398-9995; 1398-9995
• DOI: 10.1111/all.12021

Background Caveolin‐1 has emerged as a critical regulator of signaling pathways involved in lung fibrosis and inflammation. Methods Therefore, we investigated whether caveolin‐1 is deficient in asthmatic patients and in a murine model of asthma. Results Immunohistochemical analyses of endobronchial biopsies showed a remarkable loss of caveolin‐1 in the lungs of asthmatic patients compared with controls. This loss was most evident in bronchial epithelial cells and associated with an increase in the expression of extracellular matrix proteins: collagen I, tenascin, and periostin. Cultured primary bronchial epithelial cells of asthmatics had lower caveolin‐1 expression compared with control cells. In addition, caveolin‐1 expression was significantly decreased in peripheral blood monocytes from asthma patients. The loss of caveolin‐1 was also observed in a mouse model for asthma (mice sensitized and challenged with aspergillus fumigatus). Conclusions To our knowledge, this is the first demonstration that the regulatory protein caveolin‐1 is reduced in patients with asthma.