krn-7000 has been researched along with Pulmonary-Fibrosis* in 2 studies
2 other study(ies) available for krn-7000 and Pulmonary-Fibrosis
Article | Year |
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Protective role of NKT cells and macrophage M2-driven phenotype in bleomycin-induced pulmonary fibrosis.
Pulmonary fibrosis is a result of an abnormal wound healing in lung tissue triggered by an excessive accumulation of extracellular matrix proteins, loss of tissue elasticity, and debit of ventilatory function. NKT cells are a major source of Th1 and Th2 cytokines and may be crucial in the polarization of M1/M2 macrophages in pulmonary fibrogenesis. Although there appears to be constant scientific progress in that field, pulmonary fibrosis still exhibits no current cure. From these facts, we hypothesized that NKT cells could influence the development of pulmonary fibrosis via modulation of macrophage activation. Wild type (WT) and NKT type I cell-deficient mice (Jα18 Topics: Animals; Bleomycin; Collagen; Cytokines; Disease Models, Animal; Galactosylceramides; Inflammation; Lung; Macrophages; Mice; Mice, Inbred C57BL; Mice, Knockout; Natural Killer T-Cells; Phenotype; Pulmonary Fibrosis; Th1 Cells; Th2 Cells; Transforming Growth Factor beta; Vimentin | 2018 |
Treatment with alpha-galactosylceramide attenuates the development of bleomycin-induced pulmonary fibrosis.
Pulmonary fibrosis is an end-stage disorder for which efficacious therapeutic options are not readily available. Although its pathogenesis is poorly understood, pulmonary fibrosis occurs as a result of various inflammations. NKT cells modulate inflammation because of their ability to produce large amounts of cytokines by stimulation with their glycolipid ligand. In the present study, we investigated the effects of alpha-galactosylceramide (alpha-GalCer), a selective NKT cell ligand, on the development of bleomycin-induced pulmonary fibrosis. Treatment of mice with alpha-GalCer prolonged their survival under bleomycin administration by attenuating the development of pulmonary fibrosis. The protective effects of alpha-GalCer were associated with an increase in the pulmonary level of IFN-gamma and a decrease in the pulmonary level of fibrogenic cytokines such as TGF-beta and connective tissue growth factor. The initial pulmonary inflammation caused by bleomycin was also attenuated by alpha-GalCer with the reduction of the macrophage inflammatory protein-2 level. The protective effects of alpha-GalCer were markedly reduced in mice lacking NKT cells or as a result of treatment with anti-IFN-gamma Ab. These results suggest that alpha-GalCer suppresses bleomycin-induced acute pulmonary inflammation and thus attenuates the development of pulmonary fibrosis possibly by regulating several cytokine levels. Topics: Acute Disease; Adjuvants, Immunologic; Animals; Anti-Inflammatory Agents, Non-Steroidal; Antibodies, Monoclonal; Bleomycin; Chemokine CXCL2; Chemokines; Connective Tissue Growth Factor; Disease Models, Animal; Galactosylceramides; Immediate-Early Proteins; Injections, Intraperitoneal; Intercellular Signaling Peptides and Proteins; Interferon-gamma; Intubation, Intratracheal; Killer Cells, Natural; Lung; Mice; Mice, Inbred C57BL; Mice, Knockout; Pulmonary Fibrosis; T-Lymphocyte Subsets | 2004 |