Abstract
Background: Idiopathic pulmonary fibrosis is a chronic, progressive lung disease characterized by fibroproliferative matrix molecule accumulation, collagen deposition and apoptosis. Activated leukocyte cell-adhesion molecule (ALCAM; CD166) is a cell adhesion molecule that has been implicated in adhesive and migratory attribution including leukocyte homing and trafficking and the cancer metastasis. We investigated the involvement of ALCAM on development of bleomycin-induced pulmonary fibrosis in murine model. Methods: Bleomycin-induced pulmonary fibrosis model was established with wild type and ALCAM-/- mice. Pulmonary fibrosis was also induced in TGF- β transgenic mice that conditionally overexpress TGF-β upon doxycycline administration. Levels of ALCAM were measured in lung tissue and bronchial alveolar lavage fluid (BALF) of wild type mice and TGF- β transgenic mice. Histopathologic investigation was assessed and ashcroft score was rated. Quantification of BALF protein, collagen deposition in lung tissue and real-time PCR were evaluated. Result: The protein and mRNA levels of ALCAM were decreased in the BALF and lung tissue of bleomycin-treated wild type mice. Reduced ALCAM level was observed in BALF of doxycycline administered TGF-β transgenic mice relative to those of control mice. ALCAM-/- mice showed aggravated lung fibrosis response compared with wild type mice upon bleomycin treatment. Doxycycline administration derived fibrosis also exacerbated in ALCAM-/- TGF- β transgenic mice compared to wild type TGF- β transgenic mice. Conclusion: ALCAM contributes to bleomycin-induced pulmonary fibrosis associated with TGF-β response.
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