Cerebral Inflammatory Response after Fetal Asphyxia and Hyperoxic Resuscitation in Newborn Sheep.
(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)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/168143
- author
- Markus, Tina
LU
; Hansson, Stefan
LU
; Amer-Wåhlin, Isis LU ; Hellström-Westas, Lena LU ; Didrik Saugstad, Ola and Ley, David LU
- organization
- publishing date
- 2007
- 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
- 2022-02-18 08:19:31
@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 < 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.}}, 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}}, }