The immune response after hypoxia-ischemia in a mouse model of preterm brain injury

• DOI: 10.1186/s12974-014-0153-z
• Publication Date: 2014-09-04T19:33:55Z
• Authors: Anna-Maj Albertsson; Dan Bi; Luqi Duan; Xiaoli Zhang; Jianmei W Leavenw...; Lili Qiao; Changlian Zhu; Susanna Cardell; Harvey Cantor; Henrik Hagberg; Carina Mallard; Xiaoyang Wang
• Keywords: Periventricular leukomalacia

Preterm brain injury consists primarily of periventricular leukomalacia accompanied by elements gray-matter injury, and these injuries are associated with cerebral palsy cognitive impairments. Inflammation is believed to be an important contributing factor injuries. The aim this study was examine the immune response in a postnatal day (PND) 5 mouse model preterm induced hypoxia-ischemia (HI) that characterized focal white injury. C57Bl/6 mice at PND were subjected unilateral HI left carotid artery ligation subsequent exposure 10% O2 for 50 minutes, 70 or 80 minutes. At seven days post-HI, white/gray-matter examined. responses after examined different time points using RT-PCR immunohistochemical staining. minutes local white-matter cortical hippocampal atrophy, features similar those seen human infants. resulted small percentage animals being injured, produced extensive infarction multiple areas. Various responses, including changes transcription factors cytokines T-helper (Th)1/Th17-type response, increased number CD4+ T-cells, elevated levels triggering receptor expressed on myeloid cells 2 (TREM-2) its adaptor protein DNAX activation 12 kDa (DAP12) observed minute model. We have established reproducible produces consistent damage relevant This provides useful tool studying Both innate adaptive HI, show strong pro-inflammatory Th1/Th17-type bias. Such findings provide critical foundation future studies mechanism suggest blocking might neuroprotection