Developing brain and systemic inflammation: a “Toll-like” link with consequences

Modulating the immune response by deleting the third complement component, as in C3-deficient mice, revealed that they were, at least partly, protected from IR-induced injury to

One moderate dose of IR to the young rodent brain caused injuries that were detectable after several months, including impaired growth. We have shown that IR to the developing

The aim of the thesis was to investigate (1) the role of astrocyte activation and reactive gliosis in neonatal hypoxic-ischemic (HI) brain injury, (2) the role

The aim of the thesis was to investigate (1) the role of astrocyte activation and reactive gliosis in neonatal hypoxic-ischemic (HI) brain injury, (2) the role

the reduction in tissue loss, the injury to MBP and neurofilaments was also attenuated in MMP-9 deficient animals, which is similar to studies of focal cerebral ischemia in

The overall aim of this thesis was to study the expression of TLRs in the immature brain, choroid plexus and endothelial cells after inflammatory stimuli and/or HI, and to

In support, it has been shown that activation of TLR4 in the adult mouse can induce neuroinflammation independent of peripheral inflammation suggesting that activation of TLR4 at

Our results suggest that systemic activation of TLR2 suppresses mitochondrial respiration and exacerbates HI induced brain injury.. Inflammation is present whether perinatal