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Condition: Asthma

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Total 404 results found since Jan 2013.

Evaluation of nasal epithelium sampling as a tool in the preclinical development of siRNA‐based therapeutics for asthma
Abstract The development of siRNA‐based asthma therapeutics is currently hampered by a paucity of relevant biomarkers and the need to ascertain tissue‐specific gene targeting in the context of active disease. Epithelial STAT6 expression is fundamental to asthma pathogenesis in which inflammatory changes are found throughout the respiratory tract. Therefore, to improve preclinical evaluation, we tested the efficacy of STAT6‐targeting siRNA within nasal epithelial cells (NEC's) obtained from asthmatic and non‐asthmatic donors. STAT6 expression was invariant in both donor groups and amenable to suppression by siRNA tr...
Source: Journal of Cellular and Molecular Medicine - February 13, 2013 Category: Molecular Biology Authors: Gareth D Healey, Neil Evans, Julian M Hopkin, Gwyneth Davies, William Walker Tags: Original Article Source Type: research

LATE-BREAKING ABSTRACT: Inhibition of the ubiquitin-E3-ligase FBXW7 enhances steroid efficacy: New concept for treating steroid insensitivity
Conclusion: Reduction of FBXW7 caused a significant augmentation of functional GR and may have the potential to improve the efficacy of steroids.
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Kaestle, M., Wyatt, D., Nicklin, P. Tags: 5.3 Allergy and Immunology Source Type: research

SOCS1 Regulates IL-4-induced IRS-2 Signaling in Human Monocytes Signal Transduction
Allergic asthma is a chronic lung disease initiated and driven by Th2 cytokines IL-4/-13. In macrophages, IL-4/-13 bind IL-4 receptors, which signal through insulin receptor substrate (IRS)-2, inducing M2 macrophage differentiation. M2 macrophages correlate with disease severity and poor lung function, although the mechanisms that regulate M2 polarization are not understood. Following IL-4 exposure, suppressor of cytokine signaling (SOCS)1 is highly induced in human monocytes. We found that siRNA knockdown of SOCS1 prolonged IRS-2 tyrosine phosphorylation and enhanced M2 differentiation, although siRNA knockdown of SOCS3 d...
Source: Journal of Biological Chemistry - September 22, 2016 Category: Chemistry Authors: McCormick, S. M., Gowda, N., Fang, J. X., Heller, N. M. Tags: Immunology Source Type: research

Suppressor of Cytokine Signaling (SOCS)1 Regulates Interleukin-4 (IL-4)-activated Insulin Receptor Substrate (IRS)-2 Tyrosine Phosphorylation in Monocytes and Macrophages via the Proteasome Signal Transduction
Allergic asthma is a chronic lung disease initiated and driven by Th2 cytokines IL-4/-13. In macrophages, IL-4/-13 bind IL-4 receptors, which signal through insulin receptor substrate (IRS)-2, inducing M2 macrophage differentiation. M2 macrophages correlate with disease severity and poor lung function, although the mechanisms that regulate M2 polarization are not understood. Following IL-4 exposure, suppressor of cytokine signaling (SOCS)1 is highly induced in human monocytes. We found that siRNA knockdown of SOCS1 prolonged IRS-2 tyrosine phosphorylation and enhanced M2 differentiation, although siRNA knockdown of SOCS3 d...
Source: Journal of Biological Chemistry - September 22, 2016 Category: Chemistry Authors: Sarah M. McCormick, Nagaraj Gowda, Jessie X. Fang, Nicola M. Heller Tags: Immunology Source Type: research

Ribosomal protein S3 gene silencing protects against experimental allergic asthma
We reported here for the first time that RPS3 gene silencing ameliorates experimental allergic asthma, probably via interruption of NF-B activity, confirming RPS3 a novel therapeutic target for the treatment of allergic airway inflammation.
Source: European Respiratory Journal - November 7, 2016 Category: Respiratory Medicine Authors: Dong, J., Liao, W., Peh, H. Y., Chan, T. K., Tan, W. S. D., Li, L., Wong, W. S. F. Tags: 5.3 Allergy and Immunology Source Type: research

Increased CTGF expression of circulating fibrocytes in asthmatic patients with severe OSA - the role of HIF-1a and HDAC7
Conclusion: Severe OSA related hypoxia increases CTGF expression in circulating fibrocytes via activation of HIF-1α that requires HDAC7 nuclear co-transprotation. HDAC7 may serve a therapeutic target for airway remodeling in asthmatics with severe OSA.
Source: European Respiratory Journal - November 19, 2018 Category: Respiratory Medicine Authors: Wang, T.-Y., Lo, Y.-L., Wang, C.-H., Kuo, H.-P. Tags: Airway Cell Biology and Immunopathology Source Type: research

Mucin 1 downregulation impairs the anti-necroptotic effects of glucocorticoids in human bronchial epithelial cells
Publication date: Available online 7 February 2019Source: Life SciencesAuthor(s): Huojun Zhang, Qian Liu, Luxia Kong, Shuyun XuAbstractAimsTo investigate whether mucin 1 (MUC1) downregulation reduced the sensitivity of tumor necrosis factor-alpha (TNF-α)-induced bronchial epithelial cells to glucocorticoid-mediated necroptosis and explore the underlying mechanisms.Main methodsThe human lung bronchial epithelial cell line (16HBE) was transfected with small interfering RNA (siRNA) against MUC1 and then stimulated by TNF-α, where some cells were pretreated with dexamethasone. Flow cytometry was performed to analyze necropto...
Source: Life Sciences - February 7, 2019 Category: Biology Source Type: research

Transcriptional and Epigenetic Modulation of Human Rhinovirus-Induced CXCL10 Production by Cigarette Smoke.
Abstract Human rhinovirus (HRV) triggers exacerbations of asthma and chronic obstructive pulmonary disease (COPD). Cigarette smoking is the primary risk factor for the development of COPD and 25% of asthmatics smoke. Smokers experience both longer and more severe colds. We previously showed that cigarette smoke extract (CSE) inhibited HRV-induced expression of a range of epithelial antiviral molecules. Here, we use CXCL10 as a model antiviral gene to examine the mechanisms by which CSE inhibits epithelial antiviral immunity. HRV-induced CXCL10 transcription depends upon activation of nuclear factor-ĸB (NF-ĸB) an...
Source: American Journal of Respiratory Cell and Molecular Biology - October 15, 2013 Category: Molecular Biology Authors: Hudy MH, Traves SL, Proud D Tags: Am J Respir Cell Mol Biol Source Type: research

The Plant Derivative Compound A Inhibits the Production of Corticosteroid-resistant Chemokines by Airway Smooth Muscle Cells.
Abstract Preclinical models of human conditions including asthma showed the therapeutic potential of compound A (CpdA), a dissociated glucocorticoid (GC) receptor (GRα) ligand. Whether CpdA inhibits GC resistance, a central feature of severe asthma, has not been addressed. We investigated whether CpdA modulates cytokine-induced GC resistance in human airway smooth muscle (ASM) cells. Healthy and asthmatic ASM cells were treated with TNFα/IFNγ for 24 hr in the presence or absence of CpdA. ELISA and qPCR assays were used to assess the effect of CpdA on chemokine expression. Activation of GRα by CpdA was assessed...
Source: Am J Respir Cell Mol... - April 21, 2015 Category: Respiratory Medicine Authors: Gavrila A, Chachi L, Tliba O, Brightling C, Amrani Y Tags: Am J Respir Cell Mol Biol Source Type: research

Protocadherin-1 binds to SMAD3 and suppresses TGFβ1-induced gene transcription.
In conclusion, we demonstrate that PCDH1 binds to SMAD3 and regulates its activation by TGF-β signaling in bronchial epithelial cells. We propose that PCDH1 and SMAD3 act in a single pathway in asthma susceptibility that affects the sensitivity of the airway epithelium to TGF-β. PMID: 26209277 [PubMed - as supplied by publisher]
Source: Am J Physiol Lung Ce... - July 24, 2015 Category: Respiratory Medicine Authors: Faura Tellez G, Vandepoele K, Brouwer U, Koning H, Elderman RM, Hackett TL, Willemse BW, Holloway J, Van Roy F, Koppelman GH, Nawijn MC Tags: Am J Physiol Lung Cell Mol Physiol Source Type: research

Protocadherin-1 binds to SMAD3 and suppresses TGF-{beta}1-induced gene transcription
In conclusion, we demonstrate that PCDH1 binds to SMAD3 and regulates its activation by TGF-β signaling in bronchial epithelial cells. We propose that PCDH1 and SMAD3 act in a single pathway in asthma susceptibility that affects sensitivity of the airway epithelium to TGF-β.
Source: AJP: Lung Cellular and Molecular Physiology - October 1, 2015 Category: Respiratory Medicine Authors: Faura Tellez, G., Vandepoele, K., Brouwer, U., Koning, H., Elderman, R. M., Hackett, T.-L., Willemse, B. W. M., Holloway, J., Van Roy, F., Koppelman, G. H., Nawijn, M. C. Tags: ARTICLES Source Type: research

p300 and C/EBP β-regulated IKKβ expression are involved in thrombin-induced IL-8/CXCL8 expression in human lung epithelial cells
In this study, we aimed to investigate the roles of p300 and C/EBPβ-reliant IKKβ expression in thrombin-induced IL-8/CXCL8 expression. Thrombin-induced increases in IL-8/CXCL8-luciferase activity and IL-8/CXCL8 release were inhibited by p300 small interfering (siRNA). Thrombin-caused histone H3 acetylation was attenuated by p300 siRNA. Stimulation of cells with thrombin for 12h resulted in increases in IKKβ expression and phosphorylation in human lung epithelial cells. However, thrombin did not affect p65 expression. Moreover, 12h of thrombin stimulation produced increases in IKKβ expression and phosphorylation, and I...
Source: Pharmacological Research - April 26, 2017 Category: Drugs & Pharmacology Source Type: research

PINX1 and TERT Are Required for TNF- α-Induced Airway Smooth Muscle Chemokine Gene Expression.
In this study, we sought to address two key questions: whether telomerase is involved in inflammation in ASM cells, and whether components of the shelterin complex are also required for an inflammatory response in ASM cells. Telomerase inhibitors and telomerase small interfering RNA (siRNA) reduced TNF-α-induced chemokine expression in ASM cells. Telomerase siRNA and inhibitors reduced NF-κB activity. An siRNA screen of shelterin components identified a requirement for PIN2/TERF1 interacting-telomerase inhibitor 1 (PINX1) in chemokine gene expression. High-level PINX1 overexpression reduced NF-κB reporter activity, but ...
Source: Journal of Immunology - January 5, 2018 Category: Allergy & Immunology Authors: Deacon K, Knox AJ Tags: J Immunol Source Type: research

Silencing of Gal-7 inhibits TGF- β1-induced apoptosis of human airway epithelial cells through JNK signaling pathway.
In this study, we investigated the expression and role of Gal-7 in the apoptosis of bronchial epithelial cells BEAS-2B upon TGF-β1 stimulation. TGF-β1 significantly induced apoptosis of BEAS-2B cells, as determined by flow cytometry. Western blot results revealed that the mRNA and protein expression of Gal-7 were obviously increased after TGF-β1 stimulation. Small interfering RNA (siRNA)-mediated knockdown of Gal-7 abrogated TGF-β1-evoked cell apoptosis. Simultaneously, increased Bcl-2 expression, decreased Bax expression and the cleavage of poly ADP-ribose polymerase (PARP) and caspase-3 activity were also monitored i...
Source: Experimental Cell Research - December 27, 2018 Category: Cytology Authors: Sun X, Zhang W Tags: Exp Cell Res Source Type: research

Immune-Modulation by the Human Respiratory Syncytial Virus: Focus on Dendritic Cells
This study is complemented by another report that found that hRSV infection induces significant expression of three miRNAs, namely hsa-miR-4448, hsa-miR-30a-5p, and hsa-miR-4634 in human DCs (104). Interestingly, this latter study also performed comparative analyses of miRNA profiles between DCs infected with hRSV and a related virus, namely the human metapneumovirus, and found that both viruses induced the expression of elevated levels of hsa-miR-4634. Elucidating the contribution of these miRNAs in DCs in response to hRSV remains to be determined. Dendritic Cell Phenotype and Migration Upon hRSV Infection in vivo Altho...
Source: Frontiers in Immunology - April 14, 2019 Category: Allergy & Immunology Source Type: research