SESSION TYPE: ILD Posters
PRESENTED ON: Wednesday, October 24, 2012 at 01:30 PM - 02:30 PM
PURPOSE: We hypothesized that increased pulmonary vascular permeability may play a role in the pathogenesis of acute exacerbation of idiopathic interstitial pneumonias (AE-IIP). Angiopoietin-1 (Ang-1) promotes endothelial stabilization and quiescence, whereas angiopoietin-2 (Ang-2) promotes endothelial activation, destabilization, and inflammation. We examined whether angiopoietin expression would be associated with the pathogenesis of AE-IIP.
METHODS: Eighteen patients with AE-IIP, 21 patients with acute lung injury/acute respiratory distress syndrome (ALI/ARDS), 25 patients with stable state of idiopathic interstitial pneumonias (SS-IIP), and 20 healthy volunteers (HV) were enrolled. Circulating and bronchoalveolar lavage fluid (BALF) levels of Ang-1 and Ang-2 were measured by an enzyme-linked immunosolbent assay. An immunohistochemistry was performed to demonstrate the expression of Ang-1 and Ang-2.
RESULTS: Circulating levels of Ang-1 in patients with AE-IIP were significantly lower than those in SS-IIP or HV, whereas circulating Ang-2 levels in patients with AE-IIP tended to be high when compared with SS-IIP or HV. The ratio of Ang-2/Ang-1 in patients with AE-IIP was significantly higher than that in patients with SS-IIP or HV. Serum Ang-1 in ALI/ARDS was lower and Ang-2 was higher than those in SS-IIP or HV. There was a positive correlation between serum levels of Ang-1 and KL-6 in patients with AE-IIP. BALF Ang-2 concentrations of AE-IIP were significantly higher than those of SS-IIP. Immunohistochemistry disclosed that Ang-2 was expressed on vascular endothelial cells and hypertrophic type-2 epithelial cells.
CONCLUSIONS: Increased pulmonary vascular permeability due to angiopoietin may play a role in the pathogenesis of AE-IIP.
CLINICAL IMPLICATIONS: This study would reinforce the hypothesis that the pathogenesis of AE-IIP may be similar to that of ALI/ARDS.
DISCLOSURE: The following authors have nothing to disclose: Masaru Ando, Eishi Miyazaki, Tetsutaro Abe, Chihiro Ehara, Akihiro Goto, Taiki Masuda, Suehiro Nishio, Hideaki Fujisaki, Mari Yamasue, Toshihiro Ishii, Takeo Ito, Ryuichi Takenaka, Shin-ichi Nureki, Toshihide Kumamoto
No Product/Research Disclosure InformationOita University Faculty of Medicine, Yufu, Japan