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Cerebral Inflammatory Response after Fetal Asphyxia and Hyperoxic Resuscitation in Newborn Sheep.

Markus, Tina LU ; Hansson, Stefan LU orcid ; Amer-Wåhlin, Isis LU ; Hellström-Westas, Lena LU ; Didrik Saugstad, Ola and Ley, David LU (2007) In Pediatric Research 62. p.71-77
Abstract
Resuscitation with pure oxygen at birth after fetal asphyxia may aggravate brain damage by inducing pro-inflammation. The toll-like receptors (TLRs) may serve a pro-inflammatory role in hyperoxemia during ischemia-reperfusion. Sixteen near-term fetal sheep (132-136 d) were subjected to 10 min of cord occlusion, delivery and mechanical ventilation with 100% O-2 (n = 8), or 21% O-2 (n = 8) for 30 min followed by normoxemia for 90 min. Eight sheep fetuses were delivered immediately with inspired O-2 targeted at normoxemia for 120 min (controls). Levels and distributions of mRNAs for IL-1 beta, TNF-alpha, IL-12p40, IL-18, IL-6, IL-10, IFN-gamma, TLR-2. -3 and -4 in cerebral tissue at 2 h after birth were evaluated with real-time polymerase... (More)
Resuscitation with pure oxygen at birth after fetal asphyxia may aggravate brain damage by inducing pro-inflammation. The toll-like receptors (TLRs) may serve a pro-inflammatory role in hyperoxemia during ischemia-reperfusion. Sixteen near-term fetal sheep (132-136 d) were subjected to 10 min of cord occlusion, delivery and mechanical ventilation with 100% O-2 (n = 8), or 21% O-2 (n = 8) for 30 min followed by normoxemia for 90 min. Eight sheep fetuses were delivered immediately with inspired O-2 targeted at normoxemia for 120 min (controls). Levels and distributions of mRNAs for IL-1 beta, TNF-alpha, IL-12p40, IL-18, IL-6, IL-10, IFN-gamma, TLR-2. -3 and -4 in cerebral tissue at 2 h after birth were evaluated with real-time polymerase chain reaction (PCR) and in situ hybridization. Expressions of IL-1 beta, IL-12p40, TLR-2, and TLR-4 were increased in cortex/subcortex after resuscitation with 100% 02 compared with 21% O-2 (all p < 0.05) and to controls (all p < 0.05). Increased cellular expression of IL-1 beta was localized to sub-meningeal cortical layers and to sub-cortical white matter. Hyperoxic resuscitation at birth following fetal asphyxia induces a cerebral pro-inflammatory response with an up-regulation of TLR-2 and -4. These may be early events leading to increased tissue damage after exposure to hyperoxemia at birth. (Less)
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author
; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Pediatric Research
volume
62
pages
71 - 77
publisher
International Pediatric Foundation Inc.
external identifiers
  • wos:000247641300014
  • scopus:34250852881
ISSN
1530-0447
language
English
LU publication?
yes
id
30d2f558-f98c-42d9-ae8d-89ae3be5778f (old id 168143)
alternative location
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17519806&dopt=Abstract
date added to LUP
2016-04-01 11:59:49
date last changed
2025-10-14 09:10:13
@article{30d2f558-f98c-42d9-ae8d-89ae3be5778f,
  abstract     = {{Resuscitation with pure oxygen at birth after fetal asphyxia may aggravate brain damage by inducing pro-inflammation. The toll-like receptors (TLRs) may serve a pro-inflammatory role in hyperoxemia during ischemia-reperfusion. Sixteen near-term fetal sheep (132-136 d) were subjected to 10 min of cord occlusion, delivery and mechanical ventilation with 100% O-2 (n = 8), or 21% O-2 (n = 8) for 30 min followed by normoxemia for 90 min. Eight sheep fetuses were delivered immediately with inspired O-2 targeted at normoxemia for 120 min (controls). Levels and distributions of mRNAs for IL-1 beta, TNF-alpha, IL-12p40, IL-18, IL-6, IL-10, IFN-gamma, TLR-2. -3 and -4 in cerebral tissue at 2 h after birth were evaluated with real-time polymerase chain reaction (PCR) and in situ hybridization. Expressions of IL-1 beta, IL-12p40, TLR-2, and TLR-4 were increased in cortex/subcortex after resuscitation with 100% 02 compared with 21% O-2 (all p &lt; 0.05) and to controls (all p &lt; 0.05). Increased cellular expression of IL-1 beta was localized to sub-meningeal cortical layers and to sub-cortical white matter. Hyperoxic resuscitation at birth following fetal asphyxia induces a cerebral pro-inflammatory response with an up-regulation of TLR-2 and -4. These may be early events leading to increased tissue damage after exposure to hyperoxemia at birth.}},
  author       = {{Markus, Tina and Hansson, Stefan and Amer-Wåhlin, Isis and Hellström-Westas, Lena and Didrik Saugstad, Ola and Ley, David}},
  issn         = {{1530-0447}},
  language     = {{eng}},
  pages        = {{71--77}},
  publisher    = {{International Pediatric Foundation Inc.}},
  series       = {{Pediatric Research}},
  title        = {{Cerebral Inflammatory Response after Fetal Asphyxia and Hyperoxic Resuscitation in Newborn Sheep.}},
  url          = {{http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=17519806&dopt=Abstract}},
  volume       = {{62}},
  year         = {{2007}},
}