Barry W. McColl

TL;DR: It is found that microglia have distinct region-dependent transcriptional identities and age in a regionally variable manner, and in the young adult brain, differences in bioenergetic and immunoregulatory pathways were the major sources of heterogeneity and suggested that cerebellar and hippocampalmicroglia exist in a more immune-vigilant state.

TL;DR: The data show for the first time that an acute systemic inflammatory stimulus is detrimental to outcome after experimental stroke and highlight IL-1 as a critical mediator in this paradigm, and suggestIL-1-induced potentiation of neutrophil mobilization via CXC chemokine induction is a putative mechanism underlying this effect.

TL;DR: Interestingly, the more severe injury associated with 60 mins of MCAo leads to a markedly reduced proliferation of resident microglial cells, suggesting that these cells may play a protective function, possibly through phagocytosis of infiltrating neutrophils, which further support possible beneficial actions of microglia cells in the injured brain.

TL;DR: An overview of the impact of systemic inflammation on stroke susceptibility and outcome is provided and potential mechanisms underlying the impact on ischemic brain injury are discussed to highlight the implications for stroke prevention, therapy and modeling.

TL;DR: Data indicate that a transformation from transient to sustained BBB disruption caused by enhanced neutrophil-derived neurovascular MMP-9 activity is a critical mechanism underlying the exacerbation of ischemic brain injury by systemic inflammation.