Abstract

The alveolar epithelium responds to injury by upregulation of various specialized functions: proliferation and differentiation of epithelial cells, maintenance of electroyte and water balance, secretion of surfactant and associated proteins, and metabolism of xenobiotics and toxins. Genes upregulated during lung epithelial injury caused by a variety of environmental agents may serve as sensitive biomarkers of mild epithelial damage thus allowing for timely intervention. We have developed two monoclonal antibodies (2A3 and 3F9) directed to freshly isolated alveolar type II (ATII) cells 1 Miller YE Walker SR Spencer JS et al. Monoclonal antibodies specific for antigens expressed by rat type II alveolar epithelial and nonciliated bronchiolar cells.. Exp Lung Res. 1989; 15: 635-649 Crossref PubMed Scopus (13) Google Scholar which identify alveolar epithelial antigens with highly upregulated expression in two rat models of lung epithelial injury: hyperoxia and radiation exposure. The 2A3 monoclonal antibody identifies by enzyme-linked immunosorbent assay (ELISA) and immunofluorescence freshly isolated and early-cultured ATII cells but fails to identify the antigen in lung in vivo. Since 2A3 expression occurred only during the process of isolation and culture of ATII cells, we hypothesized that ATII cell exposure to other stressful conditions, such as lung injury models, would also lead to upregulated expression of this antigen.

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