Hydrogen sulfide protects against bleomycin-induced pulmonary fibrosis in rats by inhibiting NF-κB expression and regulating Th1/Th2 balance

Cao, Hua; Zhou, Xin; Zhang, Jianping; Huang, Xinli; Zhang, Yu; Zhang, Xintong; Chu, Li

doi:10.1016/j.toxlet.2013.11.008

Cited by 52 publications

(53 citation statements)

References 35 publications

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“…In ALI, neutrophils are the earliest immune cells which recruited to the site of injury and express multiple cytotoxic products. In LPS or BLE-induced ALI, the neutrophils accumulated in the lungs, changed the production of pro-inflammatory cytokines and subsequently led to the pulmonary injury [24,25]. In this study, we found the neutrophils evidently increased in lung tissues after LPS or BLE exposure.…”

Section: Discussionsupporting

confidence: 48%

Platycodin D attenuates acute lung injury by suppressing apoptosis and inflammation in vivo and in vitro

Tao

Wang

et al. 2015

International Immunopharmacology

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Section: Discussionsupporting

confidence: 48%

Platycodin D attenuates acute lung injury by suppressing apoptosis and inflammation in vivo and in vitro

Tao

Wang

et al. 2015

International Immunopharmacology

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“…NaHS administration inhibited NF-B activation in a mouse model of hemorrhagic shock as well as in a rat model of acute lung injury. Similarly, H 2 S donor treatment in a rat model of bleomycininduced pulmonary inflammation and fibrosis led to the inhibition of activation of the NF-B subunit p65 (44). In vitro, NaHS and GYY4137 have been shown to inhibit LPS-induced NF-B activation in cultured macrophages (5).…”

Section: Discussionmentioning

confidence: 96%

Role of Hydrogen Sulfide in Paramyxovirus Infections

Escaffre

et al. 2015

J Virol

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Hydrogen sulfide (H 2 S) is an endogenous gaseous mediator that has gained increasing recognition as an important player in modulating acute and chronic inflammatory diseases. However, its role in virus-induced lung inflammation is currently unknown. Respiratory syncytial virus (RSV) is a major cause of upper and lower respiratory tract infections in children for which no vaccine or effective treatment is available. Using the slow-releasing H 2 S donor GYY4137 and propargylglycin (PAG), an inhibitor of cystathionine-␥-lyase (CSE), a key enzyme that produces intracellular H 2 S, we found that RSV infection led to a reduced ability to generate and maintain intracellular H 2 S levels in airway epithelial cells (AECs). Inhibition of CSE with PAG resulted in increased viral replication and chemokine secretion. On the other hand, treatment of AECs with the H 2 S donor GYY4137 reduced proinflammatory mediator production and significantly reduced viral replication, even when administered several hours after viral absorption. GYY4137 also significantly reduced replication and inflammatory chemokine production induced by human metapneumovirus (hMPV) and Nipah virus (NiV), suggesting a broad inhibitory effect of H 2 S on paramyxovirus infections. GYY4137 treatment had no effect on RSV genome replication or viral mRNA and protein synthesis, but it inhibited syncytium formation and virus assembly/release. GYY4137 inhibition of proinflammatory gene expression occurred by modulation of the activation of the key transcription factors nuclear factor B (NF-B) and interferon regulatory factor 3 (IRF-3) at a step subsequent to their nuclear translocation. H 2 S antiviral and immunoregulatory properties could represent a novel treatment strategy for paramyxovirus infections. IMPORTANCERSV is a global health concern, causing significant morbidity and economic losses as well as mortality in developing countries. After decades of intensive research, no vaccine or effective treatment, with the exception of immunoprophylaxis, is available for this infection as well as for other important respiratory mucosal viruses. This study identifies hydrogen sulfide as a novel cellular mediator that can modulate viral replication and proinflammatory gene expression, both important determinants of lung injury in respiratory viral infections, with potential for rapid translation of such findings into novel therapeutic approaches for viral bronchiolitis and pneumonia.

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“…[44][45][46] To date, most silicosis models have only detected Th1/Th2 cells and cytokines within 28 days. 47 However, the occurrence and development of silicosis is a gradual and prolonged process, and the entire process of silicosis cannot be reected in 28 days. Therefore, we dynamically examined Th1/ Th2 cells and IFN-g and IL-4 cytokines for up to 84 days.…”

Section: 36mentioning

confidence: 99%

Dendritic cells trigger imbalance of Th1/Th2 cells in silica dust exposure rat model via MHC-II, CD80, CD86 and IL-12

et al. 2018

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Silicosis is one of the most common occupational respiratory diseases caused by inhaling silica dust over a prolonged period of time, and the progression of silicosis is accompanied with chronic inflammation and progressive pulmonary fibrosis, in which dendritic cells (DCs), the most powerful antigen presentation cell (APC) in the immune response, play a crucial role. To investigate the role of DCs in the development of silicosis, we established an experimental silicosis rat model and examined the number of DCs and alveolar macrophages (AMs) in lung tissues using immunofluorescence over 84 days. Additionally, to obtain an overview of the immunological changes in rat lung tissues, a series of indicators including Th1/Th2 cells, IFN-g, IL-4, MHC-II, CD80/86 and IL-12 were detected using flow cytometry and an enzyme-linked immunosorbent assay (ELISA) as well as a real-time polymerase chain reaction (PCR) assay. We observed that the number of DCs slightly increased at the inflammatory stage, and it increased significantly at the final stage of fibrosis. Polarization of Th1 cells and IFN-g expressions were dominant during the inflammatory stage, whereas polarization of Th2 cells and IL-4 expressions were dominant during the fibrotic stage. The subsequent mechanistic study found that the expressions of MHC-II, CD80/86 and IL-12, which are the key molecules that connect DCs and Th cells, changed dynamically in the experimental silicosis rat model. The data obtained in this study indicated that the increase in DCs may contribute to polarization of Th1/Th2 cells via MHC-II, CD80/86, and IL-12 in silica dust-exposed rats.

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Hydrogen sulfide protects against bleomycin-induced pulmonary fibrosis in rats by inhibiting NF-κB expression and regulating Th1/Th2 balance

Cited by 52 publications

References 35 publications

Platycodin D attenuates acute lung injury by suppressing apoptosis and inflammation in vivo and in vitro

Platycodin D attenuates acute lung injury by suppressing apoptosis and inflammation in vivo and in vitro

Role of Hydrogen Sulfide in Paramyxovirus Infections

Dendritic cells trigger imbalance of Th1/Th2 cells in silica dust exposure rat model via MHC-II, CD80, CD86 and IL-12

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