The Role of Inflammation in the Pathogenesis of Idiopathic Pulmonary Fibrosis

Bringardner, Benjamin D.; Baran, Christopher P.; Eubank, Timothy D.; Marsh, Clay B.

doi:10.1089/ars.2007.1897

Cited by 257 publications

(199 citation statements)

References 151 publications

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“…This finding further suggests that Doxy restores the balance of epithelial-mesenchymal cells by inhibiting the TGF-β signaling pathway and suppressing oxidative stress and inflammation to alleviate epithelial cell injury. Inflammation plays a role in disease genesis and progression in both human IPF and murine models of PF (30). In this study, we analyzed the effect of Doxy on inflammation by evaluating the levels of inflammatory cytokines in mouse plasma.…”

Section: Discussionmentioning

confidence: 99%

Doxycycline attenuates paraquat-induced pulmonary fibrosis by downregulating the TGF-β signaling pathway

Hua

et al. 2017

J. Thorac. Dis.

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Background: Paraquat (PQ) is a highly efficient herbicide that remains widely used in agriculture.However, the inappropriate application of this herbicide may cause multiple organ injuries including pulmonary injury. In this study, we report that doxycycline (Doxy) treats PQ-induced pulmonary fibrosis (PF).Methods: Mice with PQ-induced PF were treated with different doses of Doxy by intragastric administration. Human lung cancer cell line A549 pre-treated with TGF-β1 (5 ng/mL) were treated with Doxy hydrochloride (3.4 μM). Results: PF was observed from day 28 in PQ-treated group and Doxy treatments significantly reduced pulmonary coefficient, histopathological score and collagen content in a dose-dependent manner. Doxy can inhibit the expression levels of plasma inflammation cytokines at day 28 after modeling and reduced inflammatory response at early stage of PQ-induced lung injury. Immunohistochemical staining assay and proteomic analysis indicated that Doxy could restore ectopic epithelial-mesenchymal transition (EMT) induced by PQ-treatment by regulating numerous TGF-β signaling related proteins. Conclusions:The findings suggest that Doxy can restore the balance of epithelial-mesenchymal cells and attenuate PQ-induced PF by downregulating the TGF-β signaling pathway.

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Section: Discussionmentioning

confidence: 99%

Doxycycline attenuates paraquat-induced pulmonary fibrosis by downregulating the TGF-β signaling pathway

Hua

et al. 2017

J. Thorac. Dis.

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“…The pathophysiological mechanism of PF has not been fully revealed. But inflammation was thought as an important characteristic of pulmonary fibrosis and also a major reason of pulmonary fibroblast proliferation (Bringardner et al, 2008). Inflammation and the initial immune response induce secretion disorder of cytokines and chemokines.…”

Section: Discussionmentioning

confidence: 99%

“…idiopathic cases (Bringardner et al, 2008), and toll like receptor 4 (TLR4) play a critical role in inflammatory response. Recently, several researches suggested that TLR4 signaling pathway is involved in PFprocess.…”

Section: Introductionmentioning

confidence: 99%

Resveratrol inhibits rat pulmonary fibroblast proliferation through modulation of TLR4/NF-B pathway

Li¹

2013

Afr. J. Pharm. Pharmacol.

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Resveratrol shows a powerful therapeutic effect in several cardiovascular diseases and cancer. Recent studies suggest a protective role of resveratrol in pulmonary fibrosis, but the underlying mechanism remains unknown. The aim of the present study is to investigate the anti-inflammatory effect of resveratrol on pulmonary fibrosis and reveal the role of toll like receptor 4 (TLR4) signaling pathway during the process. Pulmonary fibrosis (PF) model in rats was induced by endotracheal perfusion of bleomycin (BLM). Resveratrol treatment was given for three weeks. Blood samples and lung tissues were collected for further investigation. Results showed that the level of interleukin(IL)-1 and IL-6 in blood and lung tissue were both elevated in PF rats when compared with control rats (P<0.05). Resveratrol treatment significantly decreased IL-1 and IL-6 level (P<0.05). Real-time polymerase chain reaction (PCR) and western blot both showed that TLR4 expression in lung tissue from PF rats was upregulated while resveratrol treatment significantly decreased TLR4 expression (P<0.05). Furthermore, primary rat pulmonary fibroblast was cultured. Lipopolysaccharide (LPS) induced cellular proliferation and increased TLR4 and NF-κB expression while NF-κB inhibitor BAY 11-7085 abolished the cell proliferation induced by LPS. Increased TLR4 and NF-κB expression induced by LPS incubation were both diminished by resveratrol (P<0.05). Cellular proliferation was also inhibited by resveratrol treatment. In conclusion, the anti-inflammatory effect of resveratrol may contribute its role in antiproliferation of pulmonary fibroblast and PF therapy. TLR4/NF-κB signaling pathway is also involved in the process.

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“…Controversy regarding the role of inflammation in the pathogenesis of IPF persists, 42 with the prevailing hypothesis being that inflammation does not play a major role in the pathogenesis of IPF. [43][44][45] Our data are notable because they correlate the presence of mast cells, a specific type of inflammatory cell, with slower loss of lung function in IPF patients.…”

Section: Discussionmentioning

confidence: 99%

Lung Mast Cell Density Defines A Subpopulation Of Patients With Idiopathic Pulmonary Fibrosis

Ick¹,

Chang²,

Lee³

et al. 2011

A102. Interstitial Lung Disease: Exploring the Pathobiology of Interstitial Lung Disease: What Can We Learn From Histopathology

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Aims-The relationship of mast cells to the pathogenesis of lung fibrosis remains undefined despite recognition of their presence in the lungs of patients with pulmonary fibrosis. This study was performed to characterize the relationship of mast cells to fibrotic lung diseases.Methods and results-Lung tissues from patients with idiopathic pulmonary fibrosis (IPF), chronic hypersensitivity pneumonitis (HP), systemic sclerosis (SSc)-related interstitial lung disease (ILD) and normal individuals were subjected to chymase immunostaining and the mast cell density quantified. Eosinophils were quantified by immunostaining for eosinophil peroxidase. Changes in lung function were correlated with mast cell density. Lung tissue obtained from IPF patients had a higher density of chymase-immunoreactive mast cells than that from patients with HP, SSc-related ILD or normal lungs. IPF lung tissue had a higher density of eosinophils than normal lung. There was no correlation between mast cell density and eosinophil density in IPF lung. IPF patients with high mast cell density had a slower rate of decline in forced vital capacity (FVC) than IPF patients with low mast cell density.Conclusions-Mast cell density in IPF lungs is higher than in other fibrotic lung diseases and normal lungs. Increased mast cell density in IPF may predict slower disease progression.

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The Role of Inflammation in the Pathogenesis of Idiopathic Pulmonary Fibrosis

Cited by 257 publications

References 151 publications

Doxycycline attenuates paraquat-induced pulmonary fibrosis by downregulating the TGF-β signaling pathway

Doxycycline attenuates paraquat-induced pulmonary fibrosis by downregulating the TGF-β signaling pathway

Resveratrol inhibits rat pulmonary fibroblast proliferation through modulation of TLR4/NF-B pathway

Lung Mast Cell Density Defines A Subpopulation Of Patients With Idiopathic Pulmonary Fibrosis

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