ArticleAmerican journal of respiratory and critical care medicine2010
TLR4 is necessary for hyaluronan-mediated airway hyperresponsiveness after ozone inhalation.
Article in American journal of respiratory and critical care medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 66 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
66 citing papers in PubMed, 102 citations in OpenAlex.
- Inhaled high molecular weight hyaluronan ameliorates respiratory failure in acute COPD exacerbation: a pilot study.Respiratory research · 2021Trial
- Hyaluronan Signaling Ameliorates the Epithelial Injury Response and Barrier Disruption After Ozone Exposure.Biomolecules · 2026Article
- Hyaluronan Directs Alveolar Type II Cell Response to Acute Ozone Exposure in Mice.American journal of respiratory cell and molecular biology · 2025Article
- The SARS-CoV-2 spike S1 protein induces global proteomic changes in ATII-like rat L2 cells that are attenuated by hyaluronan.American journal of physiology. Lung cellular and molecular physiology · 2023Article
- Ozone in the Development of Pediatric Asthma and Atopic Disease.Immunology and allergy clinics of North America · 2022Review
- Proteoglycans in Toll-like receptor responses and innate immunity.American journal of physiology. Cell physiology · 2022Review
- Modulation of hyaluronan signaling as a therapeutic target in human disease.Pharmacology & therapeutics · 2022Review
- Dexmedetomidine alleviates airway hyperresponsiveness and allergic airway inflammation through the TLR4/NF‑κB signaling pathway in mice.Molecular medicine reports · 2022Article
- Hyaladherins May be Implicated in Alcohol-Induced Susceptibility to Bacterial Pneumonia.Frontiers in immunology · 2022Review
- Occupational exposure to gasoline in gasoline station male attendants promotes M1 polarization in macrophages.Environmental science and pollution research international · 2022Article
- Halogen-Induced Chemical Injury to the Mammalian Cardiopulmonary Systems.Physiology (Bethesda, Md.) · 2021Review
- Hyaluronan and halogen-induced airway hyperresponsiveness and lung injury.Annals of the New York Academy of Sciences · 2020Review
- Lung macrophages: current understanding of their roles in Ozone-induced lung diseases.Critical reviews in toxicology · 2020Review
- Upregulation of airway smooth muscle calcium-sensing receptor by low-molecular-weight hyaluronan.American journal of physiology. Lung cellular and molecular physiology · 2020Article
- A modified flavonoid accelerates oligodendrocyte maturation and functional remyelination.Glia · 2020Article
- Article
- 4-Methylumbelliferyl glucuronide contributes to hyaluronan synthesis inhibition.The Journal of biological chemistry · 2019Article
- Hyaluronan interactions with innate immunity in lung biology.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- 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
6 more citing papers are in PubMed but not listed here.
Corrections and comments
- Expression of concern · 2015-09-15Unreliable Data · Unreliable Results and/or Conclusions · · comment from 2 co-authors published 7/15/2017: http://www.atsjournals.org/doi/10.1164/rccm.1962comment
- Commented on by
- Expression of concern
Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
rationaleOzone is a common environmental air pollutant that contributes to hospitalizations for respiratory illness. The mechanisms, which regulate ozone-induced airway hyperresponsiveness, remain poorly understood. We have previously reported that toll-like receptor 4 (TLR4)-deficient animals are protected against ozone-induced airway hyperresponsiveness (AHR) and that hyaluronan (HA) mediates ozone-induced AHR. However, the relation between TLR4 and hyaluronan in the airway response to ozone remains unexplored.
objectivesWe hypothesized that HA acts as an endogenous TLR4 ligand for the development of AHR after ozone-induced environmental airway injury.
methodsTLR4-deficient and wild-type C57BL/6 mice were exposed to either inhaled ozone or intratracheal HA and the inflammatory and AHR response was measured. MEASUREMENTS AND MAIN
resultsTLR4-deficient mice have similar levels of cellular inflammation, lung injury, and soluble HA levels as those of C57BL/6 mice after inhaled ozone exposure. However, TLR4-deficient mice are partially protected from AHR after ozone exposure as well as after direct intratracheal instillation of endotoxin-free low molecular weight HA. Similar patterns of TLR4-dependent cytokines were observed in the bronchial alveolar lavage fluid after exposure to either ozone or HA. Exposure to ozone increased immunohistological staining of TLR4 on lung macrophages. Furthermore, in vitro HA exposure of bone marrow-derived macrophages induced NF-kappaB and production of a similar pattern of proinflammatory cytokines in a manner dependent on TLR4.
conclusionsOur observations support the observation that extracellular matrix HA contributes to ozone-induced airways disease. Furthermore, our results support that TLR4 contributes to the biological response to HA by mediating both the production of proinflammatory cytokines and the development of ozone-induced AHR.
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What OpenQuestion holds
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.