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Sökning: WFRF:(Hagberg Henrik) > The immune response...

LIBRIS Formathandbok  (Information om MARC21)
FältnamnIndikatorerMetadata
00005541naa a2200433 4500
001oai:gup.ub.gu.se/204394
003SwePub
008240528s2014 | |||||||||||000 ||eng|
0247 a https://gup.ub.gu.se/publication/2043942 URI
0247 a https://doi.org/10.1186/s12974-014-0153-z2 DOI
040 a (SwePub)gu
041 a eng
042 9 SwePub
072 7a ref2 swepub-contenttype
072 7a art2 swepub-publicationtype
1001 a Albertsson, Anna-Maju Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology4 aut0 (Swepub:gu)xalber
2451 0a The immune response after hypoxia-ischemia in a mouse model of preterm brain injury.
264 c 2014-09-05
264 1b Springer Science and Business Media LLC,c 2014
520 a BackgroundPreterm brain injury consists primarily of periventricular leukomalacia accompanied by elements of gray-matter injury, and these injuries are associated with cerebral palsy and cognitive impairments. Inflammation is believed to be an important contributing factor to these injuries. The aim of this study was to examine the immune response in a postnatal day (PND) 5 mouse model of preterm brain injury induced by hypoxia-ischemia (HI) that is characterized by focal white and gray-matter injury.MethodsC57Bl/6 mice at PND 5 were subjected to unilateral HI induced by left carotid artery ligation and subsequent exposure to 10% O2 for 50 minutes, 70 minutes, or 80 minutes. At seven days post-HI, the white/gray-matter injury was examined. The immune responses in the brain after HI were examined at different time points after HI using RT-PCR and immunohistochemical staining.ResultsHI for 70 minutes in PND 5 mice induced local white-matter injury with focal cortical injury and hippocampal atrophy, features that are similar to those seen in preterm brain injury in human infants. HI for 50 minutes resulted in a small percentage of animals being injured, and HI for 80 minutes produced extensive infarction in multiple brain areas. Various immune responses, including changes in transcription factors and cytokines that are associated with a T-helper (Th)1/Th17-type response, an increased number of CD4+ T-cells, and elevated levels of triggering receptor expressed on myeloid cells 2 (TREM-2) and its adaptor protein DNAX activation protein of 12 kDa (DAP12) were observed using the HI 70 minute preterm brain injury model.ConclusionsWe have established a reproducible model of HI in PND 5 mice that produces consistent local white/gray-matter brain damage that is relevant to preterm brain injury in human infants. This model provides a useful tool for studying preterm brain injury. Both innate and adaptive immune responses are observed after HI, and these show a strong pro-inflammatory Th1/Th17-type bias. Such findings provide a critical foundation for future studies on the mechanism of preterm brain injury and suggest that blocking the Th1/Th17-type immune response might provide neuroprotection after preterm brain injury.
650 7a MEDICIN OCH HÄLSOVETENSKAPx Klinisk medicinx Neurologi0 (SwePub)302072 hsv//swe
650 7a MEDICAL AND HEALTH SCIENCESx Clinical Medicinex Neurology0 (SwePub)302072 hsv//eng
653 a Brain injury; Preterm; Hypoxia-ischemia; Immune response
7001 a Bi, Danu Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology4 aut
7001 a Duan, Luqiu Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology4 aut
7001 a Zhang, Xiaoliu Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology4 aut
7001 a Leavenworth, Jianmei W4 aut
7001 a Qiao, Liliu Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology4 aut
7001 a Zhu, Changlian,d 1964u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology4 aut0 (Swepub:gu)xzhuch
7001 a Cardell, Susanna,d 1959u Gothenburg University,Göteborgs universitet,Institutionen för biomedicin, avdelningen för mikrobiologi och immunologi,Institute of Biomedicine, Department of Microbiology and Immunology4 aut0 (Swepub:gu)xcarsu
7001 a Cantor, Harvey4 aut
7001 a Hagberg, Henrik,d 1955u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology4 aut0 (Swepub:gu)xhaghe
7001 a Mallard, Carina,d 1963u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology4 aut0 (Swepub:gu)xmallc
7001 a Wang, Xiaoyang,d 1965u Gothenburg University,Göteborgs universitet,Institutionen för neurovetenskap och fysiologi,Institute of Neuroscience and Physiology4 aut0 (Swepub:gu)xwanxi
7102 a Göteborgs universitetb Institutionen för neurovetenskap och fysiologi4 org
7730 t Journal of neuroinflammationd : Springer Science and Business Media LLCg 11:1q 11:1x 1742-2094
8564 u https://jneuroinflammation.biomedcentral.com/track/pdf/10.1186/s12974-014-0153-z
8564 8u https://gup.ub.gu.se/publication/204394
8564 8u https://doi.org/10.1186/s12974-014-0153-z

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