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Start Over Descriptor "house-dust mite" Journal clinical & experimental allergy
2 results on '"house-dust mite"'

1. Selective release of miRNAs via extracellular vesicles is associated with house-dust mite allergen-induced airway inflammation.

Author

Gon, Y., Maruoka, S., Inoue, T., Kuroda, K., Yamagishi, K., Kozu, Y., Shikano, S., Soda, K., Lötvall, J., and Hashimoto, S.

Subjects
*MICRORNA, *ALLERGENS, *HOUSE dust mites, *AIRWAY (Anatomy), *INFLAMMATION, *IMMUNE response, *EXOSOMES, *DISEASES
Abstract

Background MicroRNAs (miRNAs) may facilitate cell-to-cell communication via extracellular vesicles (EVs). The biological roles of miRNAs in EVs on allergic airway inflammation are unclear. Methods Airway-secreted EVs (AEVs) were isolated from bronchoalveolar lavage fluid (BALF) of control and house-dust mite (HDM) allergen-exposed HDM-sensitized mice. The expression of miRNAs in AEVs or miRNAs and mRNAs in lung tissue was analysed using miRNA microarray. Results The amount of AEV increased 8.9-fold in BALF from HDM-exposed mice compared with that from sham-control mice. HDM exposure resulted in significant changes in the expression of 139 miRNAs in EVs and 175 miRNAs in lung tissues, with 54 miRNAs being common in both samples. Expression changes of these 54 miRNAs between miRNAs in AEVs and lung tissues after HDM exposure were inversely correlated. Computational analysis revealed that 31 genes, including IL-13 and IL-5Ra, are putative targets of the miRNAs up-regulated in AEVs but down-regulated in lung tissues after HDM exposure. The amount of AEV in BALF after HDM exposure was diminished by treatment with the sphingomyelinase inhibitor GW4869. The treatment with GW4869 also decreased Th2 cytokines and eosinophil counts in BALFs and reduced eosinophil accumulation in airway walls and mucosa. Conclusion These results indicate that selective sorting of miRNA including Th2 inhibitory miRNAs into AEVs and increase release to the airway after HDM exposure would be involved in the pathogenesis of allergic airway inflammation. [ABSTRACT FROM AUTHOR]

Published
2017
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2. Airway epithelial barrier function regulates the pathogenesis of allergic asthma

Author

Irene H. Heijink, Tillie-Louise Hackett, Martijn C. Nawijn, and Groningen Research Institute for Asthma and COPD (GRIAC)

Subjects
Thymic stromal lymphopoietin, NF-KAPPA-B, Immunology, RESPIRATORY SYNCYTIAL VIRUS, TIGHT JUNCTIONS, Cell Communication, Respiratory Mucosa, Biology, OBSTRUCTIVE PULMONARY-DISEASE, Pathogenesis, Immune system, Risk Factors, immune system diseases, E-CADHERIN, HOUSE-DUST MITE, medicine, Animals, Humans, Immunology and Allergy, Genetic Predisposition to Disease, Anti-Asthmatic Agents, MESENCHYMAL TRANSITION EMT, GENOME-WIDE ASSOCIATION, Asthma, House dust mite, Epithelial Cells, Environmental Exposure, respiratory system, medicine.disease, biology.organism_classification, Epithelium, respiratory tract diseases, medicine.anatomical_structure, Gene Expression Regulation, THYMIC STROMAL LYMPHOPOIETIN, Respiratory epithelium, GROWTH-FACTOR RECEPTOR, Airway
Abstract

The integrity of the airway epithelium in patients with asthma is often disrupted, with loss of epithelial cell-cell contacts. Airway epithelial barrier dysfunction may have important implications for asthma, because structural epithelial barrier function is tightly interwoven with the ability of the epithelium to regulate the immune system. We propose that changes at the airway epithelial barrier play a central role in the sensitisation to allergens and pathogenesis of allergic asthma. Many of the recently identified susceptibility genes for asthma are expressed in airway epithelium. However, the exact mechanisms by which the expression of epithelial susceptibility genes translates into a functionally altered response to aeroallergens in asthma are still unknown. In this review, we will focus on the role of airway epithelial barrier function in the susceptibility to develop allergic asthma and discuss therapeutic strategies aimed at the epithelial barrier.

Published
2014

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