ArticlePloS one2011
Hyaluronan signaling during ozone-induced lung injury requires TLR4, MyD88, and TIRAP.
Article in PloS one, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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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
51 citing papers in PubMed, 75 citations in OpenAlex.
- ALX/FPR2 Contributes to Serum Amyloid A-Induced Lung Neutrophil Recruitment Following Acute Ozone Exposure.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Dietary curcumin alleviates intestinal damage induced by ochratoxin A in juvenile grass carp (Animal nutrition (Zhongguo xu mu shou yi xue hui) · 2024Article
- Ozone impairs endogenous compensatory responses in allergic asthma.Toxicology and applied pharmacology · 2023Article
- Cigarette smoking and air pollution exposure and their effects on cardiovascular diseases.Frontiers in public health · 2023Review
- Hyaluronic acid restored protein permeability across injured human lung microvascular endothelial cells.FASEB bioAdvances · 2022Article
- Modulation of hyaluronan signaling as a therapeutic target in human disease.Pharmacology & therapeutics · 2022Review
- Hyaladherins May be Implicated in Alcohol-Induced Susceptibility to Bacterial Pneumonia.Frontiers in immunology · 2022Review
- Review
- Ambient air pollution and endocrinologic disorders in childhood.Annals of pediatric endocrinology & metabolism · 2021Article
- Role of Innate Immune System in Environmental Lung Diseases.Current allergy and asthma reports · 2021Review
- Article
- Lung macrophages: current understanding of their roles in Ozone-induced lung diseases.Critical reviews in toxicology · 2020Review
- A modified flavonoid accelerates oligodendrocyte maturation and functional remyelination.Glia · 2020Article
- Article
- Oxidative Stress in Ozone-Induced Chronic Lung Inflammation and Emphysema: A Facet of Chronic Obstructive Pulmonary Disease.Frontiers in immunology · 2020Review
- Article
- Assessment of genetic variation among wild Alpinia nigra (Zingiberaceae) population: an approach based on molecular phylogeny.Molecular biology reports · 2019Article
- Transcriptional Effects of Ozone and Impact on Airway Inflammation.Frontiers in immunology · 2019Review
- Instillation of hyaluronan reverses acid instillation injury to the mammalian blood gas barrier.American journal of physiology. Lung cellular and molecular physiology · 2018Article
- Effect of Particulate Matter Air Pollution on Cardiovascular Oxidative Stress Pathways.Antioxidants & redox signaling · 2018Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
Ozone exposure is associated with exacerbation of reactive airways disease. We have previously reported that the damage-associated molecular pattern, hyaluronan, is required for the complete biological response to ambient ozone and that hyaluronan fragments signal through toll-like receptor 4 (TLR4). In this study, we further investigated the role of TLR4 adaptors in ozone-induced airway hyperresponsiveness (AHR) and the direct response to hyaluronan fragments (HA). Using a murine model of AHR, C57BL/6J, TLR4-/-, MyD88-/-, and TIRAP-/- mice were characterized for AHR after exposure to either ozone (1 ppm × 3 h) or HA fragments. Animals were characterized for AHR with methacholine challenge, cellular inflammation, lung injury, and production of pro-inflammatory cytokines. Ozone-exposed C57BL/6J mice developed cellular inflammation, lung injury, pro-inflammatory cytokines, and AHR, while mice deficient in TLR4, MyD88 or TIRAP demonstrated both reduced AHR and reduced levels of pro-inflammatory cytokines including TNFα, IL-1β, MCP-1, IL-6 and KC. The level of hyaluronan was increased after inhalation of ozone in each strain of mice. Direct challenge of mice to hyaluronan resulted in AHR in C57BL/6J mice, but not in TLR4-/-, MyD88-/-, or TIRAP-/- mice. HA-induced cytokine production in wild-type mice was significantly reduced in TLR4-/-, MyD88-/-, or TIRAP-/- mice. In conclusion, our findings support that ozone-induced airway hyperresponsiveness is dependent on the HA-TLR4-MyD88-TIRAP signaling pathway.
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Registered trials
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.