OBJECTIVE: A variety of inflammatory cells accumulate in the lungs of patients with interstitial lung disease. The potential for IL-8 to be released from these cells into the lungs of patients with idiopathic interstitial pneumonia (IIP), interstitial pneumonia with collagen vascular disease (IP-CVD), sarcoidosis (SAR) and hypersensitivity pneumonitis (HP) was investigated. METHODOLOGY: IL-8 levels were assessed by enzyme-linked immunosorbent assay in BAL fluid and serum, and the expression of IL-8 in the lungs of these patients was evaluated by immunohistochemistry. RESULTS: Serum IL-8 levels were significantly elevated in patients with IIP (P < 0.05) and SAR (P < 0.01). In BAL fluid, the IL-8 level was significantly higher in patients with IIP (P < 0.05), IP-CVD (P < 0.01), SAR (P < 0.01) and HP (P < 0.01). In several cases, IL-8 level correlated with neutrophil density. The IL-8 immunopositive cells were type II pulmonary epithelial cells and alveolar and interstitial macrophages in patients with IIP and IP-CVD. CONCLUSIONS: IL-8 is likely to be a key factor in the pathogenesis of fibrosis of the lung and in lung injury.
OBJECTIVE: A variety of inflammatory cells accumulate in the lungs of patients with interstitial lung disease. The potential for IL-8 to be released from these cells into the lungs of patients with idiopathic interstitial pneumonia (IIP), interstitial pneumonia with collagen vascular disease (IP-CVD), sarcoidosis (SAR) and hypersensitivitypneumonitis (HP) was investigated. METHODOLOGY:IL-8 levels were assessed by enzyme-linked immunosorbent assay in BAL fluid and serum, and the expression of IL-8 in the lungs of these patients was evaluated by immunohistochemistry. RESULTS: Serum IL-8 levels were significantly elevated in patients with IIP (P < 0.05) and SAR (P < 0.01). In BAL fluid, the IL-8 level was significantly higher in patients with IIP (P < 0.05), IP-CVD (P < 0.01), SAR (P < 0.01) and HP (P < 0.01). In several cases, IL-8 level correlated with neutrophil density. The IL-8 immunopositive cells were type II pulmonary epithelial cells and alveolar and interstitial macrophages in patients with IIP and IP-CVD. CONCLUSIONS:IL-8 is likely to be a key factor in the pathogenesis of fibrosis of the lung and in lung injury.
Authors: Joanna L Richens; Richard A Urbanowicz; Elizabeth A M Lunt; Rebecca Metcalf; Jonathan Corne; Lucy Fairclough; Paul O'Shea Journal: Respir Res Date: 2009-04-22
Authors: Ganesh Raghu; Martine Remy-Jardin; Christopher J Ryerson; Jeffrey L Myers; Michael Kreuter; Martina Vasakova; Elena Bargagli; Jonathan H Chung; Bridget F Collins; Elisabeth Bendstrup; Hassan A Chami; Abigail T Chua; Tamera J Corte; Jean-Charles Dalphin; Sonye K Danoff; Javier Diaz-Mendoza; Abhijit Duggal; Ryoko Egashira; Thomas Ewing; Mridu Gulati; Yoshikazu Inoue; Alex R Jenkins; Kerri A Johannson; Takeshi Johkoh; Maximiliano Tamae-Kakazu; Masanori Kitaichi; Shandra L Knight; Dirk Koschel; David J Lederer; Yolanda Mageto; Lisa A Maier; Carlos Matiz; Ferran Morell; Andrew G Nicholson; Setu Patolia; Carlos A Pereira; Elisabetta A Renzoni; Margaret L Salisbury; Moises Selman; Simon L F Walsh; Wim A Wuyts; Kevin C Wilson Journal: Am J Respir Crit Care Med Date: 2020-08-01 Impact factor: 30.528