2008
DOI: 10.1016/j.ajog.2007.06.035
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Microglial activation, macrophage infiltration, and evidence of cell death in the fetal brain after uteroplacental administration of lipopolysaccharide in sheep in late gestation

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Cited by 49 publications
(44 citation statements)
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“…Direct fetal infection is not required to trigger inflammation and neural injury. In fetal sheep, uteroplacental inflammation induced by endotoxins is associated with significant microglial activation and macrophage infiltration in the fetal brain (33). Similarly, in rabbits, after maternal endotoxin exposure in late gestation, motor deficit in the rabbit pups was associated with microglia activation detected by positron emission tomography imaging (34), although the observed motor deficits were mild to moderate.…”
Section: Stages Of Microglia Activation In the Immature Brainmentioning
confidence: 95%
“…Direct fetal infection is not required to trigger inflammation and neural injury. In fetal sheep, uteroplacental inflammation induced by endotoxins is associated with significant microglial activation and macrophage infiltration in the fetal brain (33). Similarly, in rabbits, after maternal endotoxin exposure in late gestation, motor deficit in the rabbit pups was associated with microglia activation detected by positron emission tomography imaging (34), although the observed motor deficits were mild to moderate.…”
Section: Stages Of Microglia Activation In the Immature Brainmentioning
confidence: 95%
“…Microglial activation has often been the first – or at least a significant – cellular event detected in and around a lesion in several animal models of developing brain injuries such as those induced by mechanical trauma, infection/inflammation, excitotoxic insults and hypoxia-ischemia [59,71,72,73,74,75,76,77,78,79,80,81,82,83,84,85,86]. Moreover, microglial activation has been demonstrated in postmortem brain specimens of premature infants with periventricular leukomalacia [87,88,89].…”
Section: Microglial Activation In the Neonatal Periodmentioning
confidence: 99%
“…Intrauterine infection is often associated with fetal hypoxia, and although either direct fetal infection or the flooding of fetal tissues (in particular, the fetal brain) by proinflammatory cytokines is usually the point of discussion [38,39,40], the placenta itself shows considerable and distinct responses to infectious agents [41,42]. Elevated IĸB phosphorylation and activation of NF-ĸB have been described in the placenta [42], and in turn, activated NF-ĸB mediates the production and release of placental proinflammatory cytokines such as interleukin-1β and tumour necrosis factor-α [42].…”
Section: Oxidative Stress and The Inflammatory Responsementioning
confidence: 99%