ArticlePloS one2013
Endotoxin Exposure during Sensitization to Blomia tropicalis Allergens Shifts TH2 Immunity Towards a TH17-Mediated Airway Neutrophilic Inflammation: Role of TLR4 and TLR2.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 36 citations in OpenAlex.
- Inflammation induced by inhaled lipopolysaccharide depends on particle size in healthy volunteers.British journal of clinical pharmacology · 2016Trial
- Mixta mediterraneensis as a novel and abundant gut symbiont of the allergen-producing domestic mite Blomia tropicalis.Experimental & applied acarology · 2024Article
- Frequent IgE recognition ofFrontiers in immunology · 2023Article
- Studies on HBcAg-rBlo t 5-21 Fusion Protein Vaccine That AlleviatesJournal of inflammation research · 2022Article
- Innate Lymphoid Cells Are Required to Induce Airway Hyperreactivity in a Murine Neutrophilic Asthma Model.Frontiers in immunology · 2022Article
- Toll-like Receptor 4 Deficiency Aggravates Airway Hyperresponsiveness and Inflammation by Impairing Neutrophil Apoptosis in a Toluene Diisocyanate-Induced Murine Asthma Model.Allergy, asthma & immunology research · 2020Article
- The role of interleukin-17 in asthma: a protective response?ERJ open research · 2020Review
- Association between endotoxin levels in dust from indoor swine housing environments and the immune responses of pigs.Journal of veterinary science · 2018Article
- Lipopolysaccharide Exposure Alleviates Asthma in Mice by Regulating Th1/Th2 and Treg/Th17 Balance.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Dual Role of Toll-like Receptors in Human and Experimental Asthma Models.Frontiers in immunology · 2018Review
- Establishment of a mouse model of lipopolysaccharide-induced neutrophilic nasal polyps.Experimental and therapeutic medicine · 2017Article
- Comparison of the roles of house dust mite allergens, ovalbumin and lipopolysaccharides in the sensitization of mice to establish a model of severe neutrophilic asthma.Experimental and therapeutic medicine · 2017Article
- TLR2 Regulates Allergic Airway Inflammation and Autophagy Through PI3K/Akt Signaling Pathway.Inflammation · 2017Article
- Blomia tropicalis-Specific TCR Transgenic Th2 Cells Induce Inducible BALT and Severe Asthma in Mice by an IL-4/IL-13-Dependent Mechanism.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Article
- Protective Effect of an Antibody against Specific Extracellular Domain of TLR2 on Agonists-Driven Inflammatory and Allergic Response.BioMed research international · 2016Article
- Type-I interferon secretion in the acute phase promotesExperimental and therapeutic medicine · 2014Article
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Experimental evidence and epidemiological studies indicate that exposure to endotoxin lipopolysaccharide (eLPS) or other TLR agonists prevent asthma. We have previously shown in the OVA-model of asthma that eLPS administration during alum-based allergen sensitization blocked the development of lung TH2 immune responses via MyD88 pathway and IL-12/IFN-γ axis. In the present work we determined the effect of eLPS exposure during sensitization to a natural airborne allergen extract derived from the house dust mite Blomia tropicalis (Bt). Mice were subcutaneously sensitized with Bt allergens co-adsorbed onto alum with or without eLPS and challenged twice intranasally with Bt. Cellular and molecular parameters of allergic lung inflammation were evaluated 24 h after the last Bt challenge. Exposure to eLPS but not to ultrapure LPS (upLPS) preparation during sensitization to Bt allergens decreased the influx of eosinophils and increased the influx of neutrophils to the airways. Inhibition of airway eosinophilia was not observed in IFN-γdeficient mice while airway neutrophilia was not observed in IL-17RA-deficient mice as well in mice lacking MyD88, CD14, TLR4 and, surprisingly, TLR2 molecules. Notably, exposure to a synthetic TLR2 agonist (PamCSK4) also induced airway neutrophilia that was dependent on TLR2 and TLR4 molecules. In the OVA model, exposure to eLPS or PamCSK4 suppressed OVA-induced airway inflammation. Our results suggest that B. tropicalis allergens engage TLR4 that potentiates TLR2 signaling. This dual TLR activation during sensitization results in airway neutrophilic inflammation associated with increased frequency of lung TH17 cells. Our work highlight the complex interplay between bacterial products, house dust mite allergens and TLR signaling in the induction of different phenotypes of airway inflammation.
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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.