Increased bleomycin-induced lung injury in mice deficient in the transcription factor T-bet

American Journal of Physiology. Lung Cellular and Molecular Physiology
Jianguo XuMauricio Rojas

Abstract

The reasons for variable sensitivity among and within species to lung injury and fibrosis caused by bleomycin (BLM) are unknown. Because T helper (Th) 1 and 2 (Th1 and Th2) polarization of CD4+ T lymphocytes is one of the factors that affects the BLM response, we hypothesized that preventing expression of the Th1 transcription factor T-bet would render BLM-resistant BALB/c mice sensitive to BLM. Wild-type and T-bet-deficient (T-bet-/-) BALB/c mice were treated with BLM or saline solution intratracheally. After BLM treatment, collagen content in the lung increased twofold by day 14 in lungs from T-bet-/- mice but was unaffected in lungs from wild-type BALB/c mice. These findings were confirmed by collagen staining of histopathological sections. BLM treatment significantly increased respiratory frequency and decreased tidal volume by day 14 in T-bet-/- mice but had no effect in wild-type mice. Lung fibrosis in BLM-treated T-bet-/- mice was associated with increased circulating levels of Th2 cytokines and increased expression of the profibrotic factor transforming growth factor-beta1. Depletion of CD4+, but not CD8+, T cells in T-bet-/- mice diminished BLM-induced lung fibrosis and the expression of transforming growth factor-beta...Continue Reading

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