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Source: European Respiratory Journal
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Total 164 results found since Jan 2013.
IL-11 increases levels and activates circulating fibrocytes in different pulmonary hypertension animal models.
In conclusion, IL-11 promotes an increase of circulating fibrocytes, their adhesion to HPAECs and phenotypic switching to myofibroblast.
Source: European Respiratory Journal - December 1, 2022 Category: Respiratory Medicine Authors: Roger, I., Milara, J., Montero, P., Belhadj, N., Cortijo, J. Tags: 13.01 - Pulmonary hypertension Source Type: research
Novel strategies for genetic manipulation of human iPSC-derived organoid platforms
Conclusions: Our preliminary data demonstrates modest but successful transfection of patient iPSC-derived organoid cultures ‘in situ’ in 3D matrigel using a commercial transfection reagent. Further development of these methods will facilitate miRNA:Target gene interaction studies to complement ongoing research in iPSC organoid platforms and inform delivery of future therapeutic strategies utilising small RNA.
Source: European Respiratory Journal - December 1, 2022 Category: Respiratory Medicine Authors: Oglesby, I., De Santi, C., Schweikert, A., Cryan, S. A., Hurley, K. Tags: 03.02 - Airway cell biology and immunopathology Source Type: research
LSC 2014 abstract - Influenza infection of human lung macrophages increases PDL1 expression via autologous IFN{beta}
Lung macrophages are an important defence against influenza infection, but macrophage function can be dysregulated by infection. Recent work has shown that acute immune responses to influenza in the murine lung are regulated by PDL1 expression leading to rapid modulation of CD8+ T cell responses via the PD1 receptor1. This PD1/PDL1 pathway may modulate acute inflammatory responses to prevent tissue damage. The aim of the present study was to investigate how human macrophages regulate their PDL1 expression in response to influenza infection. Human lung and monocyte-derived macrophages (MDMs) were exposed to H3N2 X31 influen...
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Staples, K., Spalluto, C. M., McKendry, R. T., Wilkinson, T. M. A. Tags: 10.1 Respiratory Infections Source Type: research
Late-breaking abstract: The effects and mechanism of adiponectin on inhibiting pulmonary fibrosis
Conclusions Overall, these studies indicated some protective effects of APN on PQ induced pulmonary fibrosis in a dose-dependent manner. There are APN and functional AdipoR1 expressed by human WI-38 lung fibroblasts, suggesting a potential application prospect of APN for lung fibrosis.
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Yao, R., Cao, Y., He, Y.-r., Zeng, Z., Liang, Z.-a. Tags: 1.5 Diffuse Parenchymal Lung Disease Source Type: research
Loss of PTEN induced lung fibroblasts exhibiting similar pathogenic features to cancer cells in idiopathic pulmonary fibrosis
Conclusion: These findings indicate that lung fibroblasts have decreased PTEN expression in IPF. Inhibition of PTEN induced fibroblast activation and exhibiting similar pathogenic features to cancer cells.
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Geng, J., Huang, X., Dai, H. Tags: 1.5 Diffuse Parenchymal Lung Disease Source Type: research
Accelerating lung epithelial cell senescence in reduced CARM1 mice enhances elastase-induced emphysema
Emphysema, a key feature of chronic obstructive pulmonary disease is characterized by progressive destruction of pulmonary alveoli. Emphysema development involves alveolar senescence. CARM1, an arginine methyltransferase and transcriptional cofactor, methylating histone and non-histone proteins found crucial for regulating senescence (Wang, BMC Mol Biol 2013). We therefore, hypothesized that loss of CARM1 induces alveolar epithelial cell senescence and thus enhances the susceptibility to elastase-induced emphysema.Porcine pancreatic elastase (PPE) treated C57BL/6 (WT) or CARM1+/- mice were analyzed for lung function, histo...
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Sarker, R. S. J., Bohla, A., Amarie, O. V., Eickelberg, O., Yildirim, A. O. Tags: 3.3 Mechanisms of Lung Injury and Repair Source Type: research
Reduction of high mobility group nucleosome binding domain-5 protein promotes the development of emphysema
Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation which is associated with an enhanced chronic inflammation and development of emphysema. However, the mechanism by which genetic alteration contributes to empyhsema development is still barely understood. In a previous study we have detected spontaneous emphysema development in HMGN5 knockout mice (Kluger E.J., et. al., JBC 2013). The HMGN5 gene encodes a nucleosomal binding protein that competes with H1 on the nucleosome and loosens the structure of chromatin. It plays an important role in transcription, replication and the repair mechanism...
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Merthan, L., Bustin, M., Eickelberg, O., Yildirim, A. O. Tags: 3.3 Mechanisms of Lung Injury and Repair Source Type: research
Smad1 deficiency and female gender contribute to the development of pulmonary hypertension
Conclusions. These findings suggest that the presence of female hormones, coupled with Smad1 deficiency plays a role in the female susceptibility to develop PH.
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Mair, K., Yang, X., Long, L., White, K., Nilsen, M., Morrell, N., MacLean, M. R. Tags: 4.3 Pulmonary Circulation and Pulmonary Vascular Disease Source Type: research
The anti-inflammatory effects of sulforaphane are not mediated by the Nrf2 pathway
Sulforaphane (SFN) is a naturally occurring compound, found in cruciferous vegetables. SFN is a potent activator of the endogenous anti-oxidant transcription factor nuclear factor (erythroid-derived 2)-like 2 (Nrf2). Due to its anti-oxidant and anti-inflammatory properties SFN has been identified as a potential treatment for a number of diseases including chronic obstructive pulmonary (COPD). We confirmed that SFN activates of the Nrf2 pathway and induces the expression of haemoxygenase (HO)-1 and NAD(P)H:Quinone Oxireductase (NQO)-1. SFN suppressed interleukin (IL)-1b-induced and IL-1b plus oxidative stress (hydrogen pero...
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Durham, A., Jazrawi, E., Rhodes, J. A., Williams, C., Kilty, I., Barnes, P., Chung, K. F., Adcock, I. Tags: 5.1 Airway Pharmacology and Treatment Source Type: research
Elevated protein arginine methyltransferase 1 expression contributes to the pathogenesis of pulmonary fibrosis
Conclusions: Dysregulated PRMT1 expression in human lung fibroblasts may influence fibroblast behavior by both methylation of target proteins or by regulation of gene expression.
Source: European Respiratory Journal - December 23, 2014 Category: Respiratory Medicine Authors: Zakrzewicz, D., Zakrzewicz, A., Didiasova, M., Preissner, K. T., Wygrecka, M. Tags: 1.5 Diffuse Parenchymal Lung Disease Source Type: research
LSC Abstract - Regulation of regulatory T cell (Treg) function by cAMP-responsive element binding protein (CREB) and upstream microRNAs
Conclusion: The Creb/Crtc-pathway is activated in nTregs and in iTregs. Creb knockdown by siRNA or miR-17 & -21 reduced iTreg formation and might influence Treg function. A dysregulation of this pathway might contribute to chronic inflammatory diseases.
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Bartel, S., Kästle, M., Noessner, E., Eickelberg, O., Krauss-Etschmann, S. Tags: 3.2 Airway Cell Biology and Immunopathology Source Type: research
Compound A modulates steroid insensitive chemokines in airway smooth muscle cells via IRF-1 dependent and independent pathways
In conclusion, CpdA suppresses production of GC-resistant chemokines via IRF-1 dependent and independent mechanisms.Targeting CpdA sensitive pathways in ASM cells represents an alternative therapeutic approach for GC insensitivity treatment in asthma.
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Gavrila, A., Chachi, L., Tliba, O., Brightling, C., Amrani, Y. Tags: 5.1 Airway Pharmacology and Treatment Source Type: research
MUC4 overexpression correlates corticoid resistance in chronic rhinosinusitis with nasal polyps
Conclusion: MUC4 participates in the corticoid response that mediates GRα nuclear translocation. The high expression of MUC4 in patients with CRSwNP may participate in corticoid resistance.
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Contreras, S., Serrano, A., Diaz, L., Ballester, B., Banuls, P., Milara, J., Morell, A. Tags: 5.1 Airway Pharmacology and Treatment Source Type: research
Mucin 1 downregulation associates with corticoid resistance in chronic obstructive pulmonary disease and chronic rhinosinusitis with nasal polyps
Conclusion: Corticoid response that mediates GRα nuclear translocation requires MUC1-CT. The low expression of MUC1 in patients with CRSwNP or COPD may participate in corticoid resistance.
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Morell, A., Milara, J., Diaz, L., Ballester, B., Peiro, T., Gonzalez, S., Banuls, P., Cortijo, J. Tags: 5.1 Airway Pharmacology and Treatment Source Type: research
Shikonin-induced necroptosis is enhanced by the inhibition of autophagy in non-small cell lung cancer cells
In conclusion, our data indicated that shikonin treatment induced necroptosis and autophagy in NSCLC cells. In addition, inhibition of shikonin-induced autophagy enhanced necroptosis, suggesting that shikonin could be a novel therapeutic strategy against NSCLC.
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Hwang, K. E., Jeong, E. T., Kim, H. R. Tags: 11.1 Lung Cancer Source Type: research
