2017 Fiscal Year Final Research Report
The role of Heme Oxygenase-1 in neonatal sepsis using preterm mouse model
| Project/Area Number |
16H06971
|
|---|
| Research Category |
Grant-in-Aid for Research Activity Start-up
|
| Allocation Type | Single-year Grants |
|---|
| Research Field |
Embryonic/Neonatal medicine
|
|---|
| Research Institution | Kobe University |
|---|
Principal Investigator |
|
|---|
| Project Period (FY) |
2016-08-26 – 2018-03-31
|
| Keywords | neonatal sepsis / Heme oxygenase-1 / 早産児マウス敗血症モデル / mouse model / preterm sepsis / cytokine / immunity / inflammation |
|---|
| Outline of Final Research Achievements |
To induce sepsis, the cecal slurry (CS) model was applied to 4d-old mouse pups. In brief, adult cecums were harvested, and their contents were diluted with PBS-glycerol for CS stock preparations. HO-1 heterozygote (Het, HO-1+/-) and wild-type (WT) mice were administered CS IP at a dose of 2.0-mg/g (LD40 for WT mice, Fujioka et al, Shock 47:242, 2017), and then monitored for survival. To study the protective role of HO-1 induction, 30-micro mol heme/kg was given to 3d-old pups of both genotypes 24h prior to sepsis induction.
Treatment with 2.0-mg CS/g caused a significantly higher mortality in Het (85.0%) than WT (40.9%, p<0.01) pups. Most importantly, induction of HO-1 by heme significantly reduced mortality in both WT (6.3%) and Het (23.5%) pups. In addition, expression profiles measured using PCR arrays showed significant increases in cytokines in both genotypes 6h post-sepsis induction. This increase was generally attenuated in pups of both genotypes pre-treated with heme.
|
| Free Research Field |
胎児・新生児医学
|
