ArticleJournal of immunology (Baltimore, Md. : 1950)2010
Hyaluronan fragments contribute to the ozone-primed immune response to lipopolysaccharide.
Article in Journal of immunology (Baltimore, Md. : 1950), 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 It has been retracted, and should not be counted.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 20 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.
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Who cites it
20 citing papers in PubMed.
- Hyaluronidase treatment is associated with increased cytokine levels and reduced peritoneal neutrophil accumulation during LPS-induced inflammation.Frontiers in pharmacology · 2026Article
- Effects of ozone exposure on lung injury, inflammation, and oxidative stress in a murine model of nonpneumonic endotoxemia.Toxicological sciences : an official journal of the Society of Toxicology · 2024Article
- Role of Macrophages in Air Pollution Exposure Related Asthma.International journal of molecular sciences · 2022Review
- Role of Innate Immune System in Environmental Lung Diseases.Current allergy and asthma reports · 2021Review
- Bioactive hyaluronic acid fragments inhibit lipopolysaccharide-induced inflammatory responses via the Toll-like receptor 4 signaling pathway.Frontiers of medicine · 2021Article
- Lung macrophages: current understanding of their roles in Ozone-induced lung diseases.Critical reviews in toxicology · 2020Review
- Hyaluronan interactions with innate immunity in lung biology.Matrix biology : journal of the International Society for Matrix Biology · 2019Review
- Inflammasome, IL-1 and inflammation in ozone-induced lung injury.American journal of clinical and experimental immunology · 2016Review
- Select steroid hormone glucuronide metabolites can cause toll-like receptor 4 activation and enhanced pain.Brain, behavior, and immunity · 2015Article
- Beta-arrestin-2 negatively modulates inflammation response in mouse chondrocytes induced by 4-mer hyaluronan oligosaccharide.Molecular and cellular biochemistry · 2015Article
- The Rise and Fall of Hyaluronan in Respiratory Diseases.International journal of cell biology · 2015Review
- CD36 mediates endothelial dysfunction downstream of circulating factors induced by O3 exposure.Toxicological sciences : an official journal of the Society of Toxicology · 2013Article
- Inhaled birch pollen extract induces airway hyperresponsiveness via oxidative stress but independently of pollen-intrinsic NADPH oxidase activity, or the TLR4-TRIF pathway.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Glucuronic acid and the ethanol metabolite ethyl-glucuronide cause toll-like receptor 4 activation and enhanced pain.Brain, behavior, and immunity · 2013Article
- Genes of innate immunity and the biological response to inhaled ozone.Journal of biochemical and molecular toxicology · 2013Review
- Ozone enhances pulmonary innate immune response to a Toll-like receptor-2 agonist.American journal of respiratory cell and molecular biology · 2013Article
- Hyaluronan activation of the Nlrp3 inflammasome contributes to the development of airway hyperresponsiveness.Environmental health perspectives · 2012Article
- Novel roles of peroxiredoxins in inflammation, cancer and innate immunity.Journal of clinical biochemistry and nutrition · 2012Article
- Ambient ozone and pulmonary innate immunity.Immunologic research · 2011Review
- Hyaluronan signaling during ozone-induced lung injury requires TLR4, MyD88, and TIRAP.PloS one · 2011Article
Corrections and comments
- Correction · 2016-02-19Error in Materials · Investigation by Company/Institution · Results Not Reproducible · Unreliable Data · · Erin Potts is also known as Erin Potts-Kant;
- Commented on by
- Erratum issued
Authors and funding
5 authors.
Funding
Abstract
Hyaluronan is a high-molecular mass component of pulmonary extracelluar matrix, and lung injury can generate a low-molecular mass hyaluronan (HA) fragment that functions as endogenous ligand to cell surface receptors CD44 and TLR4. This leads to activation of intracellular NF-κB signaling and proinflammatory cytokine production. Based on previous information that ozone exposure causes increased HA in bronchial alveolar lavage fluid and ozone pre-exposure primes immune response to inhaled LPS, we hypothesized that HA production during ozone exposure augments the inflammatory response to LPS. We demonstrate that acute ozone exposure at 1 part per million for 3 h primes the immune response to low-dose aerosolized LPS in C57BL/6J mice, resulting in increased neutrophil recruitment into the airspaces, increased levels of protein and proinflammatory cytokines in the bronchoalveolar lavage fluid, and increased airway hyperresponsiveness. Intratracheal instillation of endotoxin-free HA (25 μg) enhances the biological response to inhaled LPS in a manner similar to ozone pre-exposure. In vitro studies using bone marrow-derived macrophages indicate that HA enhances LPS responses measured by TNF-α production, while immunofluorescence staining of murine alveolar macrophages demonstrates that HA induces TLR4 peripheralization and lipid raft colocalization. Collectively, our observations support that ozone primes macrophage responsiveness to low-dose LPS, in part, due to HA-induced TLR4 peripheralization in lung macrophages.
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