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Epithelial cell-derived transforming growth factor-�� in bleomycin-induced pulmonary injury

Journal Article


Abstract


  • We have investigated whether enhanced secretion of transforming growth factor-�� (TGF-��) by distal respiratory epithelial cells was associated with the development of bleomycin-induced pulmonary fibrosis. Type 2 pneumocyte-enriched preparations of bronchioloalveolar epithelial cells from normal mouse lung tissue released latent TGF-�� when cultured in serum-free medium. TGF-�� in culture supernatants could be detected using a sensitive enzyme immunoassay which employed enzyme complex amplification as a reporter system, as well as by a radiolabelled receptor competition assay. Exposure to bleomycin and other potentially fibrogenic stimuli in vitro did not stimulate production of TGF-�� by the epithelial cells but release was enhanced by treatment of the cells with interferon-��. Type 2 pneumocyte-enriched cell preparations obtained following induction of a pulmonary inflammatory response by administration of intratracheal bleomycin to susceptible C57BL/6 mice did not demonstrate increased release of TGF-�� in culture. However, the concentration of TGF-�� in bronchoalveolar lavage (BAL) fluids was significantly elevated compared to controls at 1 and 2 weeks after bleomycin-induced injury in these mice. No such increase was detected in BAL fluids from BALB/c mice, which are resistant to the effects of bleomycin. These results provide no support for a pathogenetic role of alveolar epithelial cell-derived TGF-�� in bleomycin-induced pulmonary fibrosis. Nevertheless, elevated levels of TGF-�� in BAL fluids may provide a marker of the progression of pulmonary injury to fibrosis. �� 1996 Blackwell Science Ltd.

Publication Date


  • 1996

Citation


  • Kumar, R. K., O'Grady, R., Maronese, S. E., & Wilson, M. R. (1996). Epithelial cell-derived transforming growth factor-�� in bleomycin-induced pulmonary injury. International Journal of Experimental Pathology, 77(3), 99-107. doi:10.1046/j.1365-2613.1996.586969.x

Scopus Eid


  • 2-s2.0-0029838602

Start Page


  • 99

End Page


  • 107

Volume


  • 77

Issue


  • 3

Place Of Publication


Abstract


  • We have investigated whether enhanced secretion of transforming growth factor-�� (TGF-��) by distal respiratory epithelial cells was associated with the development of bleomycin-induced pulmonary fibrosis. Type 2 pneumocyte-enriched preparations of bronchioloalveolar epithelial cells from normal mouse lung tissue released latent TGF-�� when cultured in serum-free medium. TGF-�� in culture supernatants could be detected using a sensitive enzyme immunoassay which employed enzyme complex amplification as a reporter system, as well as by a radiolabelled receptor competition assay. Exposure to bleomycin and other potentially fibrogenic stimuli in vitro did not stimulate production of TGF-�� by the epithelial cells but release was enhanced by treatment of the cells with interferon-��. Type 2 pneumocyte-enriched cell preparations obtained following induction of a pulmonary inflammatory response by administration of intratracheal bleomycin to susceptible C57BL/6 mice did not demonstrate increased release of TGF-�� in culture. However, the concentration of TGF-�� in bronchoalveolar lavage (BAL) fluids was significantly elevated compared to controls at 1 and 2 weeks after bleomycin-induced injury in these mice. No such increase was detected in BAL fluids from BALB/c mice, which are resistant to the effects of bleomycin. These results provide no support for a pathogenetic role of alveolar epithelial cell-derived TGF-�� in bleomycin-induced pulmonary fibrosis. Nevertheless, elevated levels of TGF-�� in BAL fluids may provide a marker of the progression of pulmonary injury to fibrosis. �� 1996 Blackwell Science Ltd.

Publication Date


  • 1996

Citation


  • Kumar, R. K., O'Grady, R., Maronese, S. E., & Wilson, M. R. (1996). Epithelial cell-derived transforming growth factor-�� in bleomycin-induced pulmonary injury. International Journal of Experimental Pathology, 77(3), 99-107. doi:10.1046/j.1365-2613.1996.586969.x

Scopus Eid


  • 2-s2.0-0029838602

Start Page


  • 99

End Page


  • 107

Volume


  • 77

Issue


  • 3

Place Of Publication