| Exposure to in utero lipopolysaccharide induces inflammation in the fetal ovine skin. | |
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MedLine Citation:
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PMID: 20923949 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Inflammation is a defensive process by which the body responds to both localized and systemic tissue damage by the induction of innate and adaptive immunity. Literature from human and animal studies links inappropriate in utero inflammation to preterm parturition and fetal injury. The pathways by which such inflammation may cause labor, however, are not fully understood. Any proinflammatory agonist in the amniotic fluid will contact the fetal skin, in its entirety, but a potential role of the fetal skin in the pathways to labor have not previously been explored. We hypothesized that the fetal skin would respond robustly to the presence of intra-amniotic lipopolysaccharide (LPS) in our ovine model of in utero inflammation. In vitro and in utero exposure of fetal ovine keratinocytes or fetal skin to Escherichia coli LPS reliably induced significant increases in interleukin 1β (IL-1β), IL-6, tumor necrosis factor α (TNF-α), and IL-8 expression. We demonstrate that, in utero, this expression requires direct exposure with LPS suggesting that the inflammation is triggered directly in the skin itself, rather than as a secondary response to a systemic stimuli and that inflammation involves Toll-like receptor (TLR) regulation and neutrophil chemotaxis in concordance with an acute inflammatory reaction. We show that this response involves multiple inflammatory mediators, TLR regulation, and localized inflammatory cell influx characteristic of an acute inflammatory reaction. These novel data strongly suggests that the fetal skin acts as an important mediator of the fetal inflammatory response and as such may contribute to preterm birth. |
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Authors:
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Matthew W Kemp; Masatoshi Saito; Ilias Nitsos; Alan H Jobe; Suhas G Kallapur; John P Newnham |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2010-10-05 |
Journal Detail:
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Title: Reproductive sciences (Thousand Oaks, Calif.) Volume: 18 ISSN: 1933-7205 ISO Abbreviation: Reprod Sci Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2010-12-23 Completed Date: 2011-04-11 Revised Date: 2011-11-29 |
Medline Journal Info:
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Nlm Unique ID: 101291249 Medline TA: Reprod Sci Country: United States |
Other Details:
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Languages: eng Pagination: 88-98 Citation Subset: IM |
Affiliation:
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School of Women's and Infants' Health, The University of Western Australia, Perth, Australia. mkemp@meddent.uwa.edu.au |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Amnion
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drug effects Animals Cells, Cultured Dermatitis, Contact / etiology* Escherichia coli Female Fetal Diseases / chemically induced* Gene Expression Immunohistochemistry Interleukin-1 / genetics Interleukin-1beta / genetics Interleukin-8 / genetics Keratinocytes / chemistry, drug effects, metabolism Lipopolysaccharides / administration & dosage* Polymerase Chain Reaction Pregnancy Premature Birth / etiology RNA, Messenger / analysis Sheep / embryology* Skin / chemistry, drug effects, embryology* Toll-Like Receptor 4 / analysis Tumor Necrosis Factor-alpha / genetics |
| Grant Support | |
ID/Acronym/Agency:
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HD 57869/HD/NICHD NIH HHS; R01 HD057869-03/HD/NICHD NIH HHS; R01 HD057869-04/HD/NICHD NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Interleukin-1; 0/Interleukin-1beta; 0/Interleukin-8; 0/Lipopolysaccharides; 0/RNA, Messenger; 0/Toll-Like Receptor 4; 0/Tumor Necrosis Factor-alpha |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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