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Regulation of Toll-like receptor 1 and -2 in neonatal mouse brain after hypoxia-ischemia.

Artikel i vetenskaplig tidskrift
Författare Linnea Stridh
Peter L P Smith
Andrew Stuart Naylor
Xiaoyang Wang
Carina Mallard
Publicerad i Journal of neuroinflammation
Volym 8
Nummer/häfte 1
Sidor 45
ISSN 1742-2094
Publiceringsår 2011
Publicerad vid Institutionen för neurovetenskap och fysiologi, sektionen för fysiologi
Institutionen för neurovetenskap och fysiologi, sektionen för klinisk neurovetenskap och rehabilitering
Sidor 45
Språk en
Länkar dx.doi.org/10.1186/1742-2094-8-45
https://gup.ub.gu.se/file/105256
Ämneskategorier Medicin och Hälsovetenskap

Sammanfattning

ABSTRACT: BACKGROUND: Hypoxic-ischemic (HI) brain injury remains a major problem in newborns, resulting in increased risk of neurological disorders. Neonatal HI triggers a broad inflammatory reaction in the brain, including activation of the innate immune system. Toll-like receptors (TLRs), which are key components of the innate immune system, are believed to play a role in adult cerebral ischemic injury. The expression of TLRs in the neonatal brain and their regulation after HI is unknown. METHODS: Wild type C57BL/6, TLR 1 knockout (KO) and TLR 2 KO mice were subjected to HI at postnatal day 9 and sacrificed 30 min, 6h, 24h or 5 days after HI. TLR mRNA expression was determined by RT-qPCR and protein and cell type localisation by immunohistochemistry (IHC). To evaluate brain injury, infarct volume was measured in the injured hemisphere. RESULTS: mRNA expression was detected for all investigated TLRs (TLR1-9), both in normal and HI exposed brains. After HI, TLR-1 was down-regulated at 30 min and up-regulated at 6h and 24h. TLR-2 was up-regulated at 6h and 24h, and TLR-7 at 24h. Both TLR-5 and TLR-8 were down-regulated at 24h and 30 min respectively. IHC showed an increase of TLR-1 in neurons in the ipsilateral hemisphere after HI. TLR-2 was constitutively expressed in astrocytes and in a population of neurons in the paraventricular nucleus in the hypothalamus. No changes in expression were detected following HI. Following HI, TLR-2 KO mice, but not TLR-1 KO, showed a decreased infarct volume compared to wild type (p= 0.0051). CONCLUSIONS: This study demonstrates that TLRs are regulated after HI in the neonatal brain. TLR-1 protein was up-regulated in injured areas of the brain but TLR-1 KO animals were not protected from HI. In contrast, TLR-2 was constitutively expressed in the brain and TLR-2 deficiency reduced HI injury. These data suggest that TLR-2, but not TLR-1, plays a role in neonatal HI brain injury.

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