ArticleAmerican journal of physiology. Lung cellular and molecular physiology2015
Hyaluronan mediates airway hyperresponsiveness in oxidative lung injury.
Article in American journal of physiology. Lung cellular and molecular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.
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The trial behind it
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Who cites it
47 citing papers in PubMed, 64 citations in OpenAlex.
- Oral hymecromone decreases hyaluronan in human study participants.The Journal of clinical investigation · 2022Trial
- 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
- Inhaled Halogen-Induced Oxidative Renal Damage and Dysfunction: A Lung Heart Kidney Axis.Comprehensive Physiology · 2026Article
- Chlorine inhalation-induced ARDS treated with noninvasive ventilation and awake prone positioning: a case report.Frontiers in medicine · 2026Article
- Connexin-hemichannels-mediated ATP release causes lung injury following chlorine inhalation.American journal of physiology. Cell physiology · 2025Article
- The Circadian Rhythm of Asthma Immune Metabolism.Journal of immunology research · 2025Review
- Article
- 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
- Low molecular weight hyaluronan inhibits lung epithelial ion channels by activating the calcium-sensing receptor.Matrix biology : journal of the International Society for Matrix Biology · 2023Article
- CPAP-induced airway hyper-reactivity in mice is modulated by hyaluronan synthase-3.Pediatric research · 2022Article
- Proteoglycans in Toll-like receptor responses and innate immunity.American journal of physiology. Cell physiology · 2022Review
- Biochemical, biophysical, and immunological characterization of respiratory secretions in severe SARS-CoV-2 infections.JCI insight · 2022Article
- Biochemical, Biophysical, and Immunological Characterization of Respiratory Secretions in Severe SARS-CoV-2 (COVID-19) Infections.medRxiv : the preprint server for health sciences · 2022Article
- The Glycobiology of Pulmonary Arterial Hypertension.Metabolites · 2022Review
- 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
- Sex differences in cardiopulmonary effects of acute bromine exposure.Toxicology research · 2021Article
- 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
Corrections and comments
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Authors and funding
11 authors at 4 institutions in 1 country.
Funding
Abstract
Chlorine (Cl2) inhalation induces severe oxidative lung injury and airway hyperresponsiveness (AHR) that lead to asthmalike symptoms. When inhaled, Cl2 reacts with epithelial lining fluid, forming by-products that damage hyaluronan, a constituent of the extracellular matrix, causing the release of low-molecular-weight fragments (L-HA, <300 kDa), which initiate a series of proinflammatory events. Cl2 (400 ppm, 30 min) exposure to mice caused an increase of L-HA and its binding partner, inter-α-trypsin-inhibitor (IαI), in the bronchoalveolar lavage fluid. Airway resistance following methacholine challenge was increased 24 h post-Cl2 exposure. Intratracheal administration of high-molecular-weight hyaluronan (H-HA) or an antibody against IαI post-Cl2 exposure decreased AHR. Exposure of human airway smooth muscle (HASM) cells to Cl2 (100 ppm, 10 min) or incubation with Cl2-exposed H-HA (which fragments it to L-HA) increased membrane potential depolarization, intracellular Ca(2+), and RhoA activation. Inhibition of RhoA, chelation of intracellular Ca(2+), blockade of cation channels, as well as postexposure addition of H-HA, reversed membrane depolarization in HASM cells. We propose a paradigm in which oxidative lung injury generates reactive species and L-HA that activates RhoA and Ca(2+) channels of airway smooth muscle cells, increasing their contractility and thus causing AHR.
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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.