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

Abstract

Caveolin-1 has emerged as a critical regulator of signaling pathways involved in lung fibrosis and inflammation. Therefore, we investigated whether caveolin-1 is deficient in asthmatic patients and in a murine model of asthma. 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). To our knowledge, this is the first demonstration that the regulatory protein caveolin-1 is reduced in patients with asthma.