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Condition: Asthma

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Total 404 results found since Jan 2013.

Sphingosine 1-phosphate Increases COX-2 Expression and PGE2 Secretion: Effects on β2-adrenergic Receptor Desensitization.
Abstract Tachyphylaxis of the β2-adrenergic receptor limits the efficacy of bronchodilatory β2-agonists in respiratory disease. Cellular studies in airway smooth muscle (ASM) have shown that inflammatory mediators and infectious stimuli reduce β2-adrenergic responsiveness in a cyclooxygenase 2 (COX-2)-mediated, prostaglandin E2 (PGE2)-dependant manner. Herein we show that sphingosine 1-phosphate (S1P), a bioactive sphingolipid that plays an important role in pathophysiology of asthma, also induces β2-adrenergic receptor desensitization in bronchial ASM cells and exerts hyporesponsiveness to β2-agonist. We tre...
Source: Am J Respir Cell Mol... - June 22, 2015 Category: Respiratory Medicine Authors: Rumzhum NN, Rahman MM, Oliver BG, Ammit AJ Tags: Am J Respir Cell Mol Biol Source Type: research

The Coagulant Factor Xa Induces PAR-1 and Annexin A2-dependent Airway Smooth Muscle Cytokine Production and Cell Proliferation.
In this study, the potential role of PAR-1 in mediating the effects of FXa on human airway smooth muscle (ASM) cell cytokine production and proliferation was investigated. FXa (5-50 nM), but not FX, stimulated increases in ASM interleukin-6 (IL-6) production and cell number after 24 and 48 h incubation respectively (P<0.05, n=5). FXa (15 nM) also stimulated increases in the levels of mRNA for cytokines (IL-6), cell cycle-related protein (cyclin D1) and pro-remodeling proteins (FGF-2, PDGF-B, CTGF, SM22 and PAI-1) after 3 h incubation (P<0.05, n=4). The actions of FXa were insensitive to inhibition by hirudin (1 U mL-...
Source: Am J Respir Cell Mol... - June 29, 2015 Category: Respiratory Medicine Authors: Schuliga M, Royce SG, Langenbach S, Berhan A, Harris T, Keenan CR, Stewart AG Tags: Am J Respir Cell Mol Biol Source Type: research

Protocadherin-1 is a glucocorticoid-responsive critical regulator of airway epithelial barrier function
Conclusion: These results suggest that PCDH1 is important for airway function as a physical barrier, and its dysfunction is involved in the pathogenesis of allergic airway inflammation. We also suggest that glucocorticoids promotes epithelial barrier integrity by inducing PCDH1.
Source: BMC Pulmonary Medicine - July 31, 2015 Category: Respiratory Medicine Authors: Yutaka KozuYasuhiro GonShuichiro MaruokaKuroda KazumichiAkiko SekiyamaHiroyuki KishiYasuyuki NomuraMinoru IkedaShu Hashimoto Source Type: research

Endothelin-1 induces VCAM-1 expression-mediated inflammation via receptor tyrosine kinases and Elk/p300 in human tracheal smooth muscle cells
The elevated level of endothelin-1 (ET-1) has been detected in the bronchoalveolar lavage of patients with severe asthma, acute lung injury, acute respiratory distress syndrome, and sepsis. ET-1 may affect vessel tone together with lung physiology and pathology. Vascular cell adhesion molecule-1 (VCAM-1) is one kind of adhesion molecules participating in the process of polymorphonuclear leukocyte transmigration and regulating the occurrence and amplification of tissue inflammation. However, the molecular mechanisms underlying ET-1-mediated expression of VCAM-1 on human tracheal smooth muscle cells (HTSMCs) were largely unk...
Source: AJP: Lung Cellular and Molecular Physiology - August 1, 2015 Category: Respiratory Medicine Authors: Lin, C.-C., Lin, W.-N., Hou, W.-C., Hsiao, L.-D., Yang, C.-M. Tags: CALL FOR PAPERS Source Type: research

Human airway smooth muscle cells secrete amphiregulin via bradykinin/COX-2/PGE2, inducing COX-2, CXCL8, and VEGF expression in airway epithelial cells
Human airway smooth muscle cells (HASMC) contribute to asthma pathophysiology through an increased smooth muscle mass and elevated cytokine/chemokine output. Little is known about how HASMC and the airway epithelium interact to regulate chronic airway inflammation and remodeling. Amphiregulin is a member of the family of epidermal growth factor receptor (EGFR) agonists with cell growth and proinflammatory roles and increased expression in the lungs of asthma patients. Here we show that bradykinin (BK) stimulation of HASMC increases amphiregulin secretion in a mechanism dependent on BK-induced COX-2 expression, increased PG...
Source: AJP: Lung Cellular and Molecular Physiology - August 1, 2015 Category: Respiratory Medicine Authors: Deacon, K., Knox, A. J. Tags: CALL FOR PAPERS Source Type: research

Rho‐kinase inhibitor fasudil reduces allergic airway inflammation and mucus hypersecretion by regulating STAT6 and NFκB
ConclusionThese findings indicate that the RhoA/Rho kinase inhibitor, fasudil, plays a negative regulatory role in allergen‐induced mucus secretion and MUC5AC expression by regulating STAT6 and NFκB.This article is protected by copyright. All rights reserved.
Source: Clinical and Experimental Allergy - August 1, 2015 Category: Allergy & Immunology Authors: Xie Tao, Luo Guangyan, Zhang Yun, Wang Xing, Wang Xiaoyun, Wu Min, Li Guoping Tags: Original Article‐Basic Mechanisms in Allergic Disease Source Type: research

House dust mite allergens mediate the activation of c‑kit in dendritic cells via Toll‑like receptor 2.
Authors: Wu W, Wang CX, Chen H, Zhou J, Zhang JZ, Gao L, Zhou HY Abstract Several studies have demonstrated that the c‑kit proto‑oncogene and its ligand, stem cell factor, are important in the development of asthma. House dust mite (HDM; Dermatophagoides pteronyssinus) allergens are a major trigger in the development and exacerbation of asthma. HDM allergens can induce the activation of c‑kit in dendritic cells (DCs), leading to the development of allergic asthma. Previous studies have demonstrated that activation of Toll‑like receptor 2 (TLR2) evokes a T helper (Th)2 immune response and promotes experim...
Source: Molecular Medicine Reports - August 6, 2015 Category: Molecular Biology Tags: Mol Med Rep Source Type: research

IFN-{gamma}-induced JAK/STAT, but not NF-{kappa}B, signaling pathway is insensitive to glucocorticoid in airway epithelial cells
Although the majority of patients with asthma are well controlled by inhaled glucocorticoids (GCs), patients with severe asthma are poorly responsive to GCs. This latter group is responsible for a disproportionate share of health care costs associated with asthma. Recent studies in immune cells have incriminated interferon- (IFN-) as a possible trigger of GC insensitivity in severe asthma; however, little is known about the role of IFN- in modulating GC effects in other clinically relevant nonimmune cells, such as airway epithelial cells. We hypothesized that IFN--induced JAK/STAT-associated signaling pathways in airway ep...
Source: AJP: Lung Cellular and Molecular Physiology - August 15, 2015 Category: Respiratory Medicine Authors: O'Connell, D., Bouazza, B., Kokalari, B., Amrani, Y., Khatib, A., Ganther, J. D., Tliba, O. Tags: CALL FOR PAPERS Source Type: research

Role of protein phosphatase 5 (PP5) in mediating corticosteroid insensitivity in airway smooth muscle (ASM) cells in severe asthma
Although the mechanisms mediating corticosteroid resistance in severe asthma are still unknown, recent evidence suggests ASM cells isolated from patients with severe asthma have a decreased insensitivity to dexamethasone (Dex) with respect to the inhibition of chemokine production. Here we investigated whether this corticosteroid insensitivity seen in ASM from severe asthmatics was due to an abnormal GR signalling pathway. We here observed that production of CCL5 and CCL11 by TNF in ASM cells from severe asthmatics (compared to healthy subjects and nonsevere asthma) was not affected by Dex or fluticasone (FP) pretreatment....
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Chachi, L., Abbasian, M., Gavrila, A., Tliba, O., Brightling, C., Amrani, Y. Tags: 3.2 Airway Cell Biology and Immunopathology Source Type: research

Egr-1 regulates muc5ac expression through activator protein-1 (AP-1) in chronic airway inflammation diseases
Conclusions: Our research indicated that mucus might be initiated by Egr-1 and regulated by Egr-1/AP-1 axis in airway epithelial cellsand this might be a pathogenic mechanism of mucus hyper-secretion in chronic airway inflammation diseases.
Source: European Respiratory Journal - October 30, 2015 Category: Respiratory Medicine Authors: Zhang, C., Wu, Y.-P., Cao, J.-F., Zhao, Y., Chen, Z.-H., Shen, H.-H. Tags: 3.2 Airway Cell Biology and Immunopathology Source Type: research

Rho‐kinase inhibitor fasudil reduces allergic airway inflammation and mucus hypersecretion by regulating STAT6 and NFκB
Conclusions and Clinical RelevanceThese findings indicate that the Rho‐A/Rho kinase inhibitor, fasudil, plays a negative regulatory role in allergen‐induced mucus secretion and MUC5AC expression by regulating STAT6 and NFκB.
Source: Clinical and Experimental Allergy - November 19, 2015 Category: Allergy & Immunology Authors: T. Xie, GY. Luo, Y. Zhang, X. Wang, XY. Wang, M. Wu, GP. Li Tags: Original Article Source Type: research

Activating protein phosphatase 2A (PP2A) enhances tristetraprolin (TTP) anti-inflammatory function in A549 lung epithelial cells.
Abstract Chronic respiratory diseases are driven by inflammation, but some clinical conditions (severe asthma, COPD) are refractory to conventional anti-inflammatory therapies. Thus, novel anti-inflammatory strategies are necessary. The mRNA destabilizing protein, tristetraprolin (TTP), is an anti-inflammatory molecule that functions to induce mRNA decay of cytokines that drive pathogenesis of respiratory disorders. TTP is regulated by phosphorylation and protein phosphatase 2A (PP2A) is responsible for dephosphorylating (and hence activating) TTP, amongst other targets. PP2A is activated by small molecules, FTY72...
Source: Cellular Signalling - January 25, 2016 Category: Cytology Authors: Rahman MM, Rumzhum NN, Hansbro PM, Morris JC, Clark AR, Verrills NM, Ammit AJ Tags: Cell Signal Source Type: research

Eosinophil resistance to glucocorticoid-induced apoptosis is mediated by the transcription factor NFIL3
Abstract The mainstay of asthma therapy, glucocorticoids (GCs) exert their therapeutic effects through the inhibition of inflammatory signaling and induction of eosinophil apoptosis. However, laboratory and clinical observations of GC-resistant asthma suggest that GCs’ effects on eosinophil viability may depend on the state of eosinophil activation. In the present study we demonstrate that eosinophils stimulated with IL-5 show impaired pro-apoptotic response to GCs. We sought to determine the contribution of GC-mediated transactivating (TA) and transrepressing (TR) pathways in modulation of activated eosinophils...
Source: Apoptosis - February 15, 2016 Category: Molecular Biology Source Type: research

Formaldehyde Induces Rho-associated Kinase Activity to Evoke Airway Hyperresponsiveness.
CONCLUSIONS: Formaldehyde induces phosphorylation of the regulatory subunit of myosin light chain phosphatase (MYPT1), independent of formaldehyde-induced Nrf-2 activation in HASM cells. The findings suggest that Rho kinase-dependent Ca(2+) sensitization pathway plays a role in in formaldehyde-induced AHR. PMID: 27149505 [PubMed - as supplied by publisher]
Source: Am J Respir Cell Mol... - May 4, 2016 Category: Respiratory Medicine Authors: Jude J, Koziol-White C, Scala J, Yoo E, Jester W, Maute C, Dalton P, Panettieri R Tags: Am J Respir Cell Mol Biol Source Type: research

Reduced transforming growth factor β1 (TGF‐β1) in the repair of airway epithelial cells of children with asthma
ConclusionOur data has highlighted the importance of TGF‐β1 in pAEC wound repair in vitro. The significantly lower levels seen in asthmatic pAEC subsequently contributes to the dysregulated repair observed in these cells.
Source: Respirology - May 23, 2016 Category: Respiratory Medicine Authors: Kak‐Ming Ling, Erika N. Sutanto, Thomas Iosifidis, Elizabeth Kicic‐Starcevich, Kevin Looi, Luke W. Garratt, Kelly M. Martinovich, Francis J. Lannigan, Darryl A. Knight, Stephen M. Stick, Anthony Kicic Tags: Original Article Source Type: research