UNASSIGNED: @entity281 can initiate or exacerbate central nervous system (CNS) pathology, even in the absence of overt invasion of bacteria into the CNS. Recent epidemiological studies have demonstrated that @entity1 survivors of @entity295 have an increased risk of long-term neurocognitive decline. There is thus a need for improved understanding of the physiological mechanisms whereby @entity697 affects the CNS. In particular, @entity4100 -dependent activation of brain microvascular endothelial cells and a resulting loss of blood-brain barrier integrity have been proposed to play an important role in the effects of systemic @entity32 on the CNS. Signaling through the vagus nerve has also been considered to be an important component of CNS responses to @entity281 . Here, we demonstrate that blood-brain barrier permeabilization and hippocampal transcriptional responses during polymicrobial @entity295 occur even in the absence of @entity4100 -dependent signaling in cerebrovascular endothelial cells. We further demonstrate that these transcriptional responses can occur without vagus nerve input. These results suggest that redundant signals mediate CNS responses in @entity295 . Either endothelial or vagus nerve activation may be individually sufficient to transmit systemic @entity32 to the central nervous system. Transcriptional activation in the forebrain in @entity295 may be mediated by @entity4100 -independent endothelial mechanisms or by non-vagal neuronal pathways.

Blood-Brain Barrier Deterioration and Hippocampal Gene Expression in Polymicrobial Sepsis: An Evaluation of Endothelial XXXX and the Vagus Nerve.

@entity1 :: ('9606', 'Species') :: ['human'] @entity32 :: ('MESH:D007249', 'Disease') :: ['inflammation'] @entity295 :: ('MESH:D018805', 'Disease') :: ['sepsis'] @entity697 :: ('MESH:D000208', 'Disease') :: ['acute sepsis'] @entity4100 :: ('4615', 'Gene') :: ['MyD88'] @entity281 :: ('MESH:D007239', 'Disease') :: ['Systemic infection', 'systemic infection']
@entity4100 :: (4615,Gene) :: ['MyD88']
