Involvement of Activated Leukocyte Cell Adhesion Molecule (ALCAM/CD166) in Pulmonary Fibrosis

Abstract

RationaleIdiopathic pulmonary fibrosis is a chronic, progressive lung disease characterized by fibroproliferative matrix molecule accumulation, collagen deposition and apoptosis, eventually resulting in pulmonary dysfunction and death. 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.MethodsBleomycin‐induced pulmonary fibrosis model was established with wild type and ALCAM knockout 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, collagen deposition were evaluated.ResultThe 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 knockout mice showed aggravated lung fibrosis response compared with wild type mice upon bleomycin treatment.ConclusionALCAM contributes to bleomycin‐induced pulmonary fibrosis associated with TGF‐β response.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.