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Enhanced arginine metabolism may counteract inflammation pathways in asthma
Science Codex High arginine levels are often observed in asthmatic individuals and may support increased production of nitric oxide, which is known to worsen airway inflammation. Medications that reduce arginine availability do not effectively treat asthma … |
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Decreased Epithelial and Plasma miR-181b-5p Expression Associates with Airway Eosinophilic Inflammation in Asthma.
Clin Exp Allergy. 2016 May 18;
Authors: Huo X, Zhang K, Yi L, Mo Y, Liang Y, Zhao J, Zhang Z, Xu Y, Zhen G
Abstract
BACKGROUND: Airway eosinophilic inflammation is a pivotal feature of asthma. Epithelial cells play critical roles in airway eosinophilia. We hypothesized that epithelial microRNAs (miRNAs) are involved in airway eosinophilia.
OBJECTIVE: This study investigated the associations between epithelial and plasma miR-181b-5p and airway eosinophilic inflammation, and the possible mechanism by which miR-181b-5p participates in eosinophilic inflammation.
METHODS: Epithelial miRNAs expression was profiled by miRNA array in 8 subjects with asthma and 4 healthy controls. Epithelial miR-181b-5p expression was confirmed by quantitative PCR in the subjects for array experiment and another cohort including 21 subjects with asthma and 10 controls. Plasma miR-181b-5p was determined by quantitative PCR in 72 subjects with asthma and 35 controls. Correlation assays between epithelial or plasma miR-181b-5p expression and airway eosinophilia were performed. The target of miR-181b-5p, SPP1, was predicted by online algorithms and verified in BEAS-2B cells. The role of miR-181b-5p in epithelial proinflammatory cytokine expression was examined in an in vitro system.
RESULTS: Epithelial miR-181b-5p expression was decreased in subjects with asthma. Epithelial miR-181b-5p levels were inversely correlated with sputum and bronchial submucosal eosinophilia. Plasma miR-181b-5p was decreased and correlated with epithelial miR-181b-5p in subjects with asthma. There was a strong inverse correlation between plasma miR-181b-5p and airway eosinophilia in subjects with asthma. Plasma miR-181b-5p was increased after inhaled corticosteroids treatment. We verified that SPP1 is a target of miR-181b-5p. In human bronchial epithelial cells, miR-181b-5p regulated IL-13-induced IL-1? and CCL11 expression by targeting SPP1. Dexamethasone restored IL-13-induced miR-181b-5p downregulation and suppressed IL-13-induced SPP1, IL-1? and CCL11 expression.
CONCLUSIONS AND CLINICAL RELEVANCE: Epithelial and plasma miR-181b-5p are potential biomarkers for airway eosinophilia in asthma. MiR-181b-5p may participate in eosinophilic airway inflammation by regulating proinflammatory cytokines expression via targeting SPP1. This article is protected by copyright. All rights reserved.
PMID: 27192552 [PubMed – as supplied by publisher]
View full post on pubmed: asthma
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Strategy for depleting immune cells implicated in asthma-associated inflammation
Science Daily Patients with asthma have chronic lung inflammation that results in sporadic narrowing of the airways and difficulty breathing. Symptoms and severity are variable among individuals; however, the cells and inflammatory factors that trigger asthmatic … |
View full post on asthma – Google News
Western Daily Press |
New therapy could reduce asthma sufferers' lung inflammation
Western Daily Press Dr Adriana Lopes da Silva, of the Federal University of Rio de Janeiro in Brazil, said: "We found a single dose of highly compacted DNA nanoparticle thymulin gene therapy effectively reduces the inflammatory and remodeling process in asthmatic lungs. |
View full post on asthma – Google News
Condition: Allergic Asthma
Intervention: Biological: Whole lung antigen challenge, segmental allergen challenge
Sponsors: University of Wisconsin, Madison; National Institutes of Health (NIH)
Not yet recruiting – verified May 2016
View full post on ClinicalTrials.gov: asthma | received in the last 14 days
Cyclooxygenase 2: its regulation, role and impact in airway inflammation.
Clin Exp Allergy. 2015 Dec 18;
Authors: Rumzhum NN, Ammit AJ
Abstract
Cyclooxygenase 2 (COX-2: official gene symbol – PTGS2) has long been regarded as playing a pivotal role in the pathogenesis of airway inflammation in respiratory diseases including asthma. COX-2 can be rapidly and robustly expressed in response to a diverse range of pro-inflammatory cytokines and mediators. Thus, increased levels of COX-2 protein and prostanoid metabolites serve as key contributors to pathobiology in respiratory diseases typified by dysregulated inflammation. But COX-2 products may not be all bad: prostanoids can exert anti-inflammatory/bronchoprotective functions in airways in addition to their pro-inflammatory actions. Herein we outline COX-2 regulation and review the diverse stimuli known to induce COX-2 in the context of airway inflammation. We discuss some of the positive and negative effects that COX-2/prostanoids can exert in in vitro and in vivo models of airway inflammation, and suggest that inhibiting COX-2 expression to repress airway inflammation may be too blunt an approach; because although it might reduce the unwanted effects of COX-2 activation, it may also negate the positive effects. Evidence suggests that prostanoids produced via COX-2 upregulation show diverse actions (and herein we focus on prostaglandin E2 as a key example); these can be either beneficial or deleterious and their impact on respiratory disease can be dictated by local concentration and specific interaction with individual receptors. We propose that understanding the regulation of COX-2 expression and associated receptor-mediated functional outcomes may reveal number of critical steps amenable to pharmacological intervention. These may prove invaluable in our quest towards future development of novel anti-inflammatory pharmacotherapeutic strategies for the treatment of airway diseases. This article is protected by copyright. All rights reserved.
PMID: 26685098 [PubMed – as supplied by publisher]
View full post on pubmed: asthma
Neurology Advisor |
Asthma-Related Inflammation Boosts Chronic Migraine Risk
Neurology Advisor HealthDay News — Asthma may increase the risk of developing chronic migraines, according to a study published in Headache. The research included 4,446 Americans. At the start of the study in 2008, the study volunteers had fewer than 15 migraines a … Asthma Tied to Increased Risk of Chronic Migraines |
View full post on asthma – Google News
Condition: Asthma
Interventions: Drug: dupilumab SAR231893/REGN668; Drug: placebo; Drug: fluticasone propionate and salmeterol; Drug: budesonide and formoterol; Drug: mometasone furoate and formoterol
Sponsors: Sanofi; Regeneron Pharmaceuticals
Not yet recruiting – verified October 2015
View full post on ClinicalTrials.gov: asthma | received in the last 14 days
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Roflumilast Reduces Airway Inflammation in Asthma Patients
Lung Disease News Inhaled corticosteroids (ICS) are recommended as the most effective treatment for asthma – ICS acts by reducing inflammation in lungs' airways and sputum production via the bronchial tubes – but their prolonged use is associated with both local and … |
View full post on asthma – Google News
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Roflumilast reduces allergen-induced airway inflammation in patients with asthma
Healio “The studies presented here show that roflumilast has no acute bronchodilator actions in patients with mild to moderate asthma,” Philip Bardin, PhD, the director of the lung and sleep unit at Monash Health in Australia, and colleagues wrote. “This … |
View full post on asthma – Google News