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Query: UMLS:C0034069 (
pulmonary fibrosis
)
7,050
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Pulmonary fibrosis
is the result of abnormal processes of repair that occur after lung injury. Transforming growth factor (TGF)-beta is a key molecule in the progression of
pulmonary fibrosis
. Although clinical use of interferon (IFN)-beta did not improve survival in patients with idiopathic pulmonary fibrosis, because some preclinical studies have suggested that
IFN-beta
is a potent inhibitor of fibrogenesis, beneficial effects of
IFN-beta
have been expected. We therefore attempted to determine effects of
IFN-beta
and investigated the mechanism of action of
IFN-beta
in bleomycin-induced
pulmonary fibrosis
. Bleomycin at Day 0 and
IFN-beta
for 4 wk were administered intravenously to ICR mice. At 28 d after bleomycin injection, histologic and chemical analysis was performed for evaluation of effects of
IFN-beta
. Tissue distribution and amounts of TGF-beta1 and thrombospondin (TSP)-1/2 were analyzed.
IFN-beta
attenuated prolylhydroxylase activity, resulting in inhibition of
pulmonary fibrosis
. Bleomycin-induced increase in TGF-beta1 in epithelial cells and extracellular matrix was attenuated by
IFN-beta
. TSP-1/2 was limited in platelets of control mice, but was present in foamy cells in fibrotic regions induced by bleomycin. These findings suggest that the antifibrotic effect of
IFN-beta
is inhibition of TGF-beta and its activation via decrease in TSP-1/2 in lung tissue and change in location of TSP-1/2 from platelets to foamy cells.
...
PMID:Interferon-{beta} inhibits bleomycin-induced lung fibrosis by decreasing transforming growth factor-{beta} and thrombospondin. 1555 19
Lung disorders induced by inhaled inorganic particles such as crystalline silica are characterized by chronic inflammation and
pulmonary fibrosis
. Here, we demonstrate the importance of type I interferon (IFN) in the development of crystalline silica-induced lung inflammation in mice, revealing that viruses and inorganic particles share similar signaling pathways. We found that instillation of silica is followed by the upregulation of
IFN-beta
and IRF-7 and that granulocytes (GR1(+)) and macrophages/dendritic cells (CD11c(+)) are major producers of type I IFN in response to silica. Two months after silica administration, both IFNAR- and IRF-7-deficient mice produced significantly less pulmonary inflammation and chemokines (KC and CCL2) than competent mice but developed similar lung fibrosis. Our data indicate that type I IFN contributes to the chronic lung inflammation that accompanies silica exposure in mice. Type I IFN is, however, dispensable in the development of silica-induced acute lung inflammation and
pulmonary fibrosis
.
...
PMID:Type I interferon signaling contributes to chronic inflammation in a murine model of silicosis. 2051 54
