| Formyl peptide receptor ligands promote wound closure in lung epithelial cells. | |
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MedLine Citation:
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PMID: 20889801 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Mitochondrial antigens released from damaged cells act as "danger signals" capable of promoting innate immune cell migration and activation via formyl peptide receptors (FPRs). Lung epithelial cells are equipped to migrate and mount innate immune responses in the context of acute lung injury. The goal of this study was to determine whether lung epithelial cells express FPRs, which are capable of responding to mitochondrial antigens to promote wound closure and inflammation. Using human Beas2B lung epithelial cells grown to confluency and subjected to linear scratch injury, it was found that mitochondrial antigens enhanced epithelial wound closure, and this phenomenon was inhibited by cyclosporin H, a selective inhibitor of FPR. Although mitochondrial antigens also promoted IL-8 release, this release was not FPR dependent and was unrelated to FPR-induced lung epithelial cell wound closure. The expression of functional FPR was confirmed in Beas2B and primary human tracheobronchial epithelial cells, particularly in lamellipodia at the leading edge of the closing wound. The expression of FPR was increased in response to TNF-α, LPS, scratch injury, and mitochondrial antigen treatment. Considered together, these data confirm that human lung epithelial cells express functional FPRs, which are capable of responding to endogenous mitochondrial danger signals, to promote wound closure. |
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Authors:
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Guohong Shao; Mark W Julian; Shengying Bao; Meghan K McCullers; Ju-Ping Lai; Daren L Knoell; Elliott D Crouser |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-10-01 |
Journal Detail:
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Title: American journal of respiratory cell and molecular biology Volume: 44 ISSN: 1535-4989 ISO Abbreviation: Am. J. Respir. Cell Mol. Biol. Publication Date: 2011 Mar |
Date Detail:
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Created Date: 2011-03-02 Completed Date: 2011-04-27 Revised Date: 2012-03-01 |
Medline Journal Info:
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Nlm Unique ID: 8917225 Medline TA: Am J Respir Cell Mol Biol Country: United States |
Other Details:
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Languages: eng Pagination: 264-9 Citation Subset: IM |
Affiliation:
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Division of Pulmonary, Allergy, Critical Care and Sleep Medicine, The Dorothy M. Davis Heart and Lung Research Institute, The Ohio State University Medical Center, Columbus, OH 43210-1252, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Antigens
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chemistry Cell Line Cell Movement Epithelial Cells / cytology* Humans Interleukin-8 / metabolism Ligands Lung / pathology* Microscopy, Fluorescence / methods Mitochondria / pathology Necrosis / pathology Receptors, Formyl Peptide / metabolism* Subcellular Fractions / metabolism Wound Healing |
| Chemical | |
Reg. No./Substance:
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0/Antigens; 0/Interleukin-8; 0/Ligands; 0/Receptors, Formyl Peptide |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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