scholarly journals Pulmonary Proteases in the Cystic Fibrosis Lung Induce Interleukin 8 Expression from Bronchial Epithelial Cells via a Heme/Meprin/Epidermal Growth Factor Receptor/Toll-like Receptor Pathway

2010 ◽  
Vol 286 (9) ◽  
pp. 7692-7704 ◽  
Author(s):  
Sonya Cosgrove ◽  
Sanjay H. Chotirmall ◽  
Catherine M. Greene ◽  
Noel G. McElvaney
Keyword(s):  
Cystic Fibrosis ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Growth Factor Receptor ◽  
Interleukin 8 ◽  
Toll Like Receptor ◽  
Bronchial Epithelial ◽  
Epidermal Growth

Immunolocalization of Transforming Growth Factor a and Epidermal Growth Factor Receptor in Lungs of Patients with Cystic Fibrosis

1999 ◽  
Vol 2 (5) ◽  
pp. 415-423 ◽  
Author(s):  
William D. Hardie ◽  
Pablo A. Bejarano ◽  
Mary Ann Miller ◽  
James R. Yankaskas ◽  
Jon H. Ritter ◽  
...  
Keyword(s):  
Cystic Fibrosis ◽  
Epidermal Growth Factor Receptor ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Lung Tissue ◽  
Transforming Growth Factor ◽  
Growth Factor Receptor ◽  
Epidermal Growth ◽  
Respiratory Epithelial

Transforming growth factor α (TGF-α) is expressed in respiratory epithelial cells and alveolar macrophages during development and following lung injury. In the present study the presence and sites of synthesis of TGF-α and its receptor, the epidermal growth factor receptor (EGF-R), were assessed in lung tissue from patients with severe lung disease caused by cystic fibrosis (CF). Lung sections from 24 individuals with CF, obtained at the time of lung transplantation, were compared to lung sections from five lung donors without CF. Cellular sites of TGF-α, EGF-R, and cellular sites of proliferation were assessed by immunohistochemistry All CF lung sections contained multiple cell types with detectable TGF-α. Compared to control sections, intensity of TGF-α immunostaining in macrophages, airway epithelial cells, and peribronchial submucosal cells was increased. EGF-R was detected in respiratory epithelial and peribronchial stromal cells but not in alveolar macrophages. The intensity of EGF-R staining in CF lung tissue did not differ from that of controls. An increased number of cells expressing Ki-67 nuclear antigen was detected in peribronchial submucosal cells but not bronchiolar epithelial cells in the CF lungs. The increased expression of TGF-α in CF lung tissue supports the concept that TGF-α plays a role in paracrine/autocrine regulation of lung remodeling associated with injury and repair in the lungs of individuals with cystic fibrosis.

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