ArticlePloS one2014
High degree of overlap between responses to a virus and to the house dust mite allergen in airway epithelial cells.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
18 citing papers in PubMed, 32 citations in OpenAlex.
- Preoperative Esketamine Alleviates Postoperative Pain after Endoscopic Plasma Adenotonsillectomy in Children.Clinical medicine & research · 2023Trial
- Combined Exposure to Ragweed and House Dust Mite Exacerbates Airway Epithelial Barrier Dysfunction: A Multimodal Approach.Medicina (Kaunas, Lithuania) · 2026Article
- NFKB1 genetic variation and allergic rhinitis susceptibility: a study in the Chinese Han population.Scientific reports · 2026Article
- An unbiased tissue transcriptome analysis identifies potential markers for skin phenotypes and therapeutic responses in atopic dermatitis.Nature communications · 2025Article
- The early-phase transcriptome and the clinical efficacy analysis in three modes of subcutaneous immunotherapy for allergic rhinitis.The World Allergy Organization journal · 2023Article
- Gene-Smoking Interaction Analysis for the Identification of Novel Asthma-Associated Genetic Factors.International journal of molecular sciences · 2023Article
- Cultured fibroblasts of the Okinawa rail present delayed innate immune response compared to that of chicken.PloS one · 2023Article
- Article
- Airway Basal Cells, Protectors of Epithelial Walls in Health and Respiratory Diseases.Frontiers in allergy · 2021Review
- House Dust Mite Exposure Causes Increased Susceptibility of Nasal Epithelial Cells to Adenovirus Infection.Viruses · 2020Article
- Airway Epithelial Dynamics in Allergy and Related Chronic Inflammatory Airway Diseases.Frontiers in cell and developmental biology · 2020Review
- TET1 contributes to allergic airway inflammation and regulates interferon and aryl hydrocarbon receptor signaling pathways in bronchial epithelial cells.Scientific reports · 2019Article
- Emerging Regulatory Roles of Dual-Specificity Phosphatases in Inflammatory Airway Disease.International journal of molecular sciences · 2019Review
- DUSP10 Negatively Regulates the Inflammatory Response to Rhinovirus through Interleukin-1β Signaling.Journal of virology · 2019Article
- Specific Induction of TSLP by the Viral RNA Analogue Poly(I:C) in Primary Epithelial Cells Derived from Nasal Polyps.PloS one · 2016Article
- Molecular mechanisms of nasal epithelium in rhinitis and rhinosinusitis.Current allergy and asthma reports · 2015Review
- Expression profiling and functional analysis of Toll-like receptors in primary healthy human nasal epithelial cells shows no correlation and a refractory LPS response.Clinical and translational allergy · 2015Article
- Functional effects of Toll-like receptor (TLR)3, 7, 9, RIG-I and MDA-5 stimulation in nasal epithelial cells.PloS one · 2014Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAirway epithelium is widely considered to play an active role in immune responses through its ability to detect changes in the environment and to generate a microenvironment for immune competent cells. Therefore, besides its role as a physical barrier, epithelium affects the outcome of the immune response by the production of various pro-inflammatory mediators.
methodsWe stimulated airway epithelial cells with viral double stranded RNA analogue poly(I:C) or with house dust mite in a time course of 24 hours. In order to determine cytokines production by stimulated cells, we performed multiplex enzyme linked immunosorbant assay (ELISA).
resultsWe demonstrate that the temporal pattern of the genes that respond to virus exposure in airway epithelium resembles to a significant degree their pattern of response to HDM. The gene expression pattern of EGR1, DUSP1, FOSL1, JUN, MYC, and IL6 is rather similar after viral (poly(I:C)) and HDM exposure. However, both triggers also induce a specific response (e.g. ATF3, FOS, and NFKB1). We confirmed these data by showing that epithelial cells produce a variety of similar mediators in response to both poly(I:C) and HDM challenge (IL1-RA, IL-17, IFN-α and MIP1-α), sometimes with a quantitative difference in response (IL2-R, IL-6, IL-8, MCP-1, MIG, and HGF). Interestingly, only four mediators (IL-12, IP-10, RANTES and VEGF) where up-regulated specifically by poly(I:C) and not by HDM. Additionally, we report that pre-exposure to HDM deregulates production of cytokines and mediators in response to poly(I:C).
conclusionsEpithelial cells responses to the HDM-allergen and a virus strongly resemble both in gene expression and in protein level explaining why these two responses may affect each other.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.