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Bleomycin-Induced Lung Injury

The Experts below are selected from a list of 1923 Experts worldwide ranked by ideXlab platform

Thomas R Ulich – 1st expert on this subject based on the ideXlab platform

  • Keratinocyte Growth Factor Decreases Pulmonary Edema, Transforming Growth Factor-Beta and Platelet-Derived Growth Factor-BB Expression, and Alveolar Type II Cell Loss in Bleomycin-Induced Lung Injury
    Inflammation, 1998
    Co-Authors: Eunhee S Yi, Moses Salgado, Scott T. Williams, Eliezer Masliah, Thomas R Ulich

    Abstract:

    Keratinocyte growth factor (KGF), a potent growth factor for type II pneumocytes and Clara cells, has been shown to prevent the end-stage pulmonary fibrosis and mortality in a rat model of Bleomycin-Induced Lung Injury. In this study, protective effects of KGF were explored during the earlier course of Bleomycin-Induced Lung Injury by studying protein exudation in alveolar edema fluids, pulmonary expression of transforming growth factor-beta (TGFβ) and platelet-derived growth factor-BB (PDGF-BB), and changes in type II pneumocytes and Clara cells after i.t. (intratracheal) bleomycin injection following KGF- or saline-pretreatment in rats. Total protein in bronchoalveolar lavage (BAL) fluids after bleomycin Injury from KGF-pretreated rats was significantly lower than the levels in saline-pretreated rats. TGFβ protein in BAL fluids which peaked at day 3 after i.t. bleomycin in saline-pretreated Lungs was not significantly increased at any time points in KGF-pretreated rats. PDGF-BB protein in whole Lung tissues of KGF-pretreated rats also remained near normal throughout the course after i.t. bleomycin, in contrast to the significant increase in saline-pretreated rats. Numbers of type II pneumocytes and Clara cells in KGF-pretreated Lungs after a high dose of bleomycin were close to the normal in intact Lungs. At the same dose of bleomycin Injury, type II pneumocytes in saline-pretreated Lungs were markedly decreased, while the number of Clara cells in these rats was relatively preserved as the pre-Injury level. In conclusion, KGF prevents Bleomycin-Induced end-stage pulmonary Injury and mortality probably at least partly by decreasing protein-rich pulmonary edema, protein expression of fibrogenic cytokines TGFβ and PDGF-BB, and type II cell loss during the course of Lung Injury.

  • keratinocyte growth factor ameliorates radiation and bleomycin induced Lung Injury and mortality
    American Journal of Pathology, 1996
    Co-Authors: Eunhee S Yi, Thomas R Ulich, Scott Williams, Denise M Malicki, Elaine M Chin, John E Tarpley

    Abstract:

    Keratinocyte growth factor (KGF) is a growth factor for type II pneumocytes. Type II pneumocyte hyperplasia, a common reaction to Lung Injury, has been postulated to play an important role in Lung repair. The potential protective effect of KGF was therefore studied in rat models of radiation- and Bleomycin-Induced Lung Injury. Intratracheal instillation of KGF (5 mg/kg) 72 and 48 hours before 18 Gy of bilateral thoracic irradiation did not significantly improve survival, although histology showed less pneumonitis and fibrosis in KGF-pretreated as compared with control-irradiated rats. Intratracheal pretreatment with KGF in rats receiving intratracheal bleomycin (2.5 U) improved survival at 3 weeks to 100% (20/20 rats) from 40% (8/20 rats) in controls. All KGF-pretreated rats receiving bleomycin were well at 3 weeks and without histological evidence of pulmonary fibrosis whereas the 8 surviving control rats exhibited severe respiratory distress. Finally, in the most lethal challenge to the Lung, rats pretreated with intratracheal KGF or saline were challenged with a combination of bleomycin (1.5 U) and bilateral thoracic irradiation (18 Gy). KGF-pretreated rats did not begin to die or show signs of respiratory distress until 7 weeks, whereas all saline-pretreated control rats receiving radiation and bleomycin died within approximately 4 weeks with severe respiratory distress and weight loss. In conclusion, radiation- and Bleomycin-Induced pulmonary Injury and respiratory death are ameliorated by KGF pretreatment, suggesting a protective role for KGF-induced type II pneumocyte proliferation in Lung Injury.

Eunhee S Yi – 2nd expert on this subject based on the ideXlab platform

  • Keratinocyte Growth Factor Decreases Pulmonary Edema, Transforming Growth Factor-Beta and Platelet-Derived Growth Factor-BB Expression, and Alveolar Type II Cell Loss in Bleomycin-Induced Lung Injury
    Inflammation, 1998
    Co-Authors: Eunhee S Yi, Moses Salgado, Scott T. Williams, Eliezer Masliah, Thomas R Ulich

    Abstract:

    Keratinocyte growth factor (KGF), a potent growth factor for type II pneumocytes and Clara cells, has been shown to prevent the end-stage pulmonary fibrosis and mortality in a rat model of Bleomycin-Induced Lung Injury. In this study, protective effects of KGF were explored during the earlier course of Bleomycin-Induced Lung Injury by studying protein exudation in alveolar edema fluids, pulmonary expression of transforming growth factor-beta (TGFβ) and platelet-derived growth factor-BB (PDGF-BB), and changes in type II pneumocytes and Clara cells after i.t. (intratracheal) bleomycin injection following KGF- or saline-pretreatment in rats. Total protein in bronchoalveolar lavage (BAL) fluids after bleomycin Injury from KGF-pretreated rats was significantly lower than the levels in saline-pretreated rats. TGFβ protein in BAL fluids which peaked at day 3 after i.t. bleomycin in saline-pretreated Lungs was not significantly increased at any time points in KGF-pretreated rats. PDGF-BB protein in whole Lung tissues of KGF-pretreated rats also remained near normal throughout the course after i.t. bleomycin, in contrast to the significant increase in saline-pretreated rats. Numbers of type II pneumocytes and Clara cells in KGF-pretreated Lungs after a high dose of bleomycin were close to the normal in intact Lungs. At the same dose of bleomycin Injury, type II pneumocytes in saline-pretreated Lungs were markedly decreased, while the number of Clara cells in these rats was relatively preserved as the pre-Injury level. In conclusion, KGF prevents Bleomycin-Induced end-stage pulmonary Injury and mortality probably at least partly by decreasing protein-rich pulmonary edema, protein expression of fibrogenic cytokines TGFβ and PDGF-BB, and type II cell loss during the course of Lung Injury.

  • keratinocyte growth factor ameliorates radiation and bleomycin induced Lung Injury and mortality
    American Journal of Pathology, 1996
    Co-Authors: Eunhee S Yi, Thomas R Ulich, Scott Williams, Denise M Malicki, Elaine M Chin, John E Tarpley

    Abstract:

    Keratinocyte growth factor (KGF) is a growth factor for type II pneumocytes. Type II pneumocyte hyperplasia, a common reaction to Lung Injury, has been postulated to play an important role in Lung repair. The potential protective effect of KGF was therefore studied in rat models of radiation- and Bleomycin-Induced Lung Injury. Intratracheal instillation of KGF (5 mg/kg) 72 and 48 hours before 18 Gy of bilateral thoracic irradiation did not significantly improve survival, although histology showed less pneumonitis and fibrosis in KGF-pretreated as compared with control-irradiated rats. Intratracheal pretreatment with KGF in rats receiving intratracheal bleomycin (2.5 U) improved survival at 3 weeks to 100% (20/20 rats) from 40% (8/20 rats) in controls. All KGF-pretreated rats receiving bleomycin were well at 3 weeks and without histological evidence of pulmonary fibrosis whereas the 8 surviving control rats exhibited severe respiratory distress. Finally, in the most lethal challenge to the Lung, rats pretreated with intratracheal KGF or saline were challenged with a combination of bleomycin (1.5 U) and bilateral thoracic irradiation (18 Gy). KGF-pretreated rats did not begin to die or show signs of respiratory distress until 7 weeks, whereas all saline-pretreated control rats receiving radiation and bleomycin died within approximately 4 weeks with severe respiratory distress and weight loss. In conclusion, radiation- and Bleomycin-Induced pulmonary Injury and respiratory death are ameliorated by KGF pretreatment, suggesting a protective role for KGF-induced type II pneumocyte proliferation in Lung Injury.

Raphael Breuer – 3rd expert on this subject based on the ideXlab platform

  • The effect of enoxaparin on Bleomycin-Induced Lung Injury in mice.
    Experimental Lung Research, 2009
    Co-Authors: Uri Laxer, Reuven Or, Ronald H. Goldstein, Izidore S. Lossos, Thomas G. Christensen, S. Gillis, Raphael Breuer

    Abstract:

    We have evaluated the effect of enoxaparin, a potent antithrombotic drug, on bleomycin (Bleo) induced pulmonary inflammation in mice. Pulmonary Injury was induced by a single intratracheal (IT) instillation of Bleo. Four groups of female C57BL/6 mice, each received one of four treatments: (1) IT Bleo and daily intraperitoneal (IP) injections of enoxaparin (EN) starting one day before IT instillation of Bleo (Bleo-EN); (2) IT Bleo and IP injections of saline (Bleo-Sal); (3) IT saline and IP enoxaparin (Sal-EN); (4) IT saline and IP saline (Sal-Sal). Animals were sacrificed 14 days after IT treatment. Lung Injury was evaluated by analysis of bronchoalveolar lavage fluid and histologically by an overall semiquantitative index of Lung Injury and a quantitative image analysis assessing alveolar wall area fraction and fibrosis fraction. Treatment of mice with enoxaparin did not ameliorate Bleo induced Lung Injury. Our study does not establish a critical role of procoagulant activity in the evolution of Bleo-ind…

  • Lymphokines in Bleomycin-Induced Lung Injury in bleomycin-sensitive C57BL/6 and -resistant BALB/c mice.
    Experimental Lung Research, 2009
    Co-Authors: Reuven Or, Michael J. Segel, Miriam Shriki, Gabriel Izbicki, Raphael Breuer

    Abstract:

    To study the pattern of lymphokines in Bleomycin-Induced Lung Injury, T cells were isolated from Lung interstitial tissue (LIL), peribronchial lymphatic tissue (PBLT), and bronchoalveolar lavage (BAL) fluid of bleomycin-“sensitive” C57Bl/6 and bleomycin-”resistant” BALB/c mice at 3, 6, and 14 days following intratracheal instillation of bleomycin or saline. After 48 hours in culture, conditioned media were collected and assayed with specific enzyme-linked immunosorbent assay (ELISA) for interferon (IFN)-, interleukin (IL)-2, IL-4 and IL-5. In bleomycin-treated C57B1/6 mice, IFN- production was increased up to 20-fold at 3 and 6 days in LIL, and at 3 days in PBLT lymphocytes. IL-4 production was slightly decreased in LIL and PBLT lymphocytes at 14 days. IL-2 and IL-5 were not changed by bleomycin. In BALB/c mice, IFN- production was increased 5-fold at 14 days, and IL-2 production at 6 days, in LIL but not PBLT. IL-4 and IL-5 were not significantly changed. The increase in IFN- may play a role in the pat…

  • Bleomycin initiates apoptosis of Lung epithelial cells by ROS but not by Fas/FasL pathway.
    American Journal of Physiology-lung Cellular and Molecular Physiology, 2005
    Co-Authors: Shulamit B. Wallach-dayan, Gabriel Izbicki, Pazit Y. Cohen, Regina Gerstl-golan, Alan Fine, Raphael Breuer

    Abstract:

    Epithelial cells are considered to be a main target of Bleomycin-Induced Lung Injury, which leads to fibrosis in vivo. We studied the characteristics of in vitro Bleomycin-Induced apoptosis in a mo…