| Hyaluronan fragments contribute to the ozone-primed immune response to lipopolysaccharide. | |
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MedLine Citation:
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PMID: 21037098 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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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Authors:
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Zhuowei Li; Erin N Potts; Claude A Piantadosi; W Michael Foster; John W Hollingsworth |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2010-10-29 |
Journal Detail:
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Title: Journal of immunology (Baltimore, Md. : 1950) Volume: 185 ISSN: 1550-6606 ISO Abbreviation: J. Immunol. Publication Date: 2010 Dec |
Date Detail:
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Created Date: 2010-11-18 Completed Date: 2011-01-10 Revised Date: 2012-03-28 |
Medline Journal Info:
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Nlm Unique ID: 2985117R Medline TA: J Immunol Country: United States |
Other Details:
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Languages: eng Pagination: 6891-8 Citation Subset: AIM; IM |
Affiliation:
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Division of Pulmonary, Allergy, and Critical Care Medicine, Department of Medicine, Duke University, Durham, NC 27710, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acute Lung Injury
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chemically induced,
immunology,
pathology Administration, Inhalation Animals Antigens, CD44 / metabolism Bone Marrow Cells / drug effects, immunology, metabolism Bronchoalveolar Lavage Fluid / chemistry, cytology, immunology Cells, Cultured Dose-Response Relationship, Immunologic Hyaluronic Acid / biosynthesis, chemistry, toxicity* Lipopolysaccharides / administration & dosage*, chemistry, pharmacology Macrophages, Alveolar / drug effects, immunology, metabolism Male Mice Mice, Inbred C57BL Molecular Weight Ozone / administration & dosage, chemistry, toxicity* |
| Grant Support | |
ID/Acronym/Agency:
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AI064789/AI/NIAID NIH HHS; AI081672/AI/NIAID NIH HHS; ES016126/ES/NIEHS NIH HHS; ES016347/ES/NIEHS NIH HHS; ES016659/ES/NIEHS NIH HHS; R01 ES016126-04/ES/NIEHS NIH HHS; R01 ES016126-05/ES/NIEHS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Antigens, CD44; 0/Lipopolysaccharides; 10028-15-6/Ozone; 9004-61-9/Hyaluronic Acid |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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