| Maternal intrauterine infection, cytokines, and brain damage in the preterm newborn. | |
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MedLine Citation:
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PMID: 9212029 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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To evaluate the hypothesis that the proinflammatory cytokines IL-1, IL-6, and tumor necrosis factor-alpha might be the link between prenatal intrauterine infection (IUI) and neonatal brain damage, the authors review the relevant epidemiologic and cytokine literature. Maternal IUI appears to increase the risk of preterm delivery, which in turn is associated with an increased risk of intraventricular hemorrhage, neonatal white matter damage, and subsequent cerebral palsy. IL-1, IL-6, and TNF-alpha have been found associated with IUI, preterm birth, neonatal infections. and neonatal brain damage. Unifying models not only postulate the presence of cytokines in the three relevant maternal/fetal compartments (uterus, fetal circulation, and fetal brain) and the ability of the cytokines to cross boundaries (placenta and blood-brain barrier) between these compartments, but also postulate how proinflammatory cytokines might lead to IVH and neonatal white matter damage during prenatal maternal infection. Interrupting the proinflammatory cytokine cascade might prevent later disability in those born near the end of the second trimester. |
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Authors:
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O Dammann; A Leviton |
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Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S.; Review |
Journal Detail:
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Title: Pediatric research Volume: 42 ISSN: 0031-3998 ISO Abbreviation: Pediatr. Res. Publication Date: 1997 Jul |
Date Detail:
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Created Date: 1997-09-09 Completed Date: 1997-09-09 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0100714 Medline TA: Pediatr Res Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 1-8 Citation Subset: IM |
Affiliation:
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Department of Neurology, Children's Hospital and Harvard Medical School, Boston, Massachusetts 02115, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Blood-Brain Barrier Brain Injuries / etiology*, immunology Cerebral Hemorrhage / etiology Cerebral Palsy / etiology Cytokines / physiology* Female Humans Infant, Newborn Infant, Premature Inflammation Mediators / physiology Interleukin-1 / physiology Interleukin-6 / physiology Leukomalacia, Periventricular / etiology Models, Biological Placenta / physiopathology Pregnancy Pregnancy Complications, Infectious / immunology* Tumor Necrosis Factor-alpha / physiology Uterine Diseases / complications, immunology |
| Grant Support | |
ID/Acronym/Agency:
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NS 27306/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Cytokines; 0/Inflammation Mediators; 0/Interleukin-1; 0/Interleukin-6; 0/Tumor Necrosis Factor-alpha |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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