The immune response after hypoxia-ischemia in a mouse model of preterm brain injury

Albertsson, Ann‐Christine; Bi, Dingren; Duan, Luqi; Zhang, Xiaoli; Leavenworth, Jianmei W.; Qiao, Lili; Zhu, Changlian; Cardell, Susanna; Cantor, Harvey; Hagberg, Henrik; Mallard, Carina; Wang, Xiaoyang

doi:10.1186/s12974-014-0153-z

Cited by 61 publications

(73 citation statements)

References 68 publications

(70 reference statements)

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“…PND3 and PND6 rat HI models have been used to resemble PVL in the immature brain (Jantzie et al, 2015; Zhu et al, 2017). In a PND5 mouse HI model, hypoxia-ischemia induces a pattern of diffuse white and focal gray matter injury similar to that in preterm infants with PVL (Albertsson et al, 2014). …”

Section: Animal Models Of Neonatal Hi Brain Injurymentioning

confidence: 97%

Brain-immune interactions in perinatal hypoxic-ischemic brain injury

Concepcion

Meng

et al. 2017

Progress in Neurobiology

184

189

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Perinatal hypoxia-ischemia remains the primary cause of acute neonatal brain injury, leading to a high mortality rate and long-term neurological deficits, such as behavioral, social, attentional, cognitive and functional motor deficits. An ever-increasing body of evidence shows that the immune response to acute cerebral hypoxia-ischemia is a major contributor to the pathophysiology of neonatal brain injury. Hypoxia-ischemia provokes an intravascular inflammatory cascade that is further augmented by the activation of resident immune cells and the cerebral infiltration of peripheral immune cells response to cellular damages in the brain parenchyma. This prolonged and/or inappropriate neuroinflammation leads to secondary brain tissue injury. Yet, the long-term effects of immune activation, especially the adaptive immune response, on the hypoxic-ischemic brain still remain unclear. The focus of this review is to summarize recent advances in the understanding of post-hypoxic-ischemic neuroinflammation triggered by the innate and adaptive immune responses and to discuss how these mechanisms modulate the brain vulnerability to injury. A greater understanding of the reciprocal interactions between the hypoxic-ischemic brain and the immune system will open new avenues for potential immunomodulatory therapy in the treatment of neonatal brain injury.

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Section: Animal Models Of Neonatal Hi Brain Injurymentioning

confidence: 97%

Brain-immune interactions in perinatal hypoxic-ischemic brain injury

Concepcion

Meng

et al. 2017

Progress in Neurobiology

184

189

View full text Add to dashboard Cite

show abstract

“…Employing murine models to study the early stages of PVL revealed the pro-inflammatory cytokines IL-1β and TNF-α, generated during the fetal inflammatory response, mediate brain injury by increasing the permeability of the blood brain barrier (BBB) to cytotoxic proteins 90, 100, 104 . This alteration in the BBB allows an abundance of stimulated macrophages to infiltrate inflamed brain tissue 90 .…”

Section: The Role Of Chorioamnionitis and Il-17 In Cerebral Palsy Andmentioning

confidence: 99%

Chorioamnionitis, IL‐17A, and fetal origins of neurologic disease

Lawrence

Wynn

2017

American J Rep Immunol

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The Centers for Disease Control and Prevention estimate that 1 in 323 infants have cerebral palsy. Highly correlated to intrauterine infection and inflammation, the incidence of cerebral palsy has remained constant over the last few decades despite significant advances in neonatal intensive care including improved ventilator techniques, surfactant therapy, maternal steroid administration, and use of intrapartum empiric antimicrobials. Recent advances in our understanding of immune responses to infection and inflammation have identified the cytokine IL-17A as a crucial component of early pro-inflammatory mediators that cause brain injury associated with neurologic impairment. Remarkably, maternal inflammatory responses to in utero inflammation and infection can also lead to potentially debilitating neurologic conditions in the offspring, which often become clinically apparent during childhood and/or early adulthood. This review details the role of IL-17A in fetal and maternal proinflammatory responses that lead to fetal brain injury and neurologic sequelae, including cerebral palsy. Recent findings regarding the role of maternal inflammatory responses in the development of childhood and adult neurologic conditions, such as autism, schizophrenia, and multiple sclerosis, will also be highlighted.

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“…Cerebral ischemia induces an inlammatory response in the brain parenchyma and systemic circulation [34,35], resulting in the augmented secretion of proinlammatory cytokines and chemotactic molecules by the vascular endothelium in newborn infants with hypoxic-ischemic injury. Hence, cytokines are important upstream efector of brain injury after ischemia [36]. Vasoregulatory mechanisms play essential roles in brain injury and tissue reperfusion in critically ill children; endothelial dysfunction results in an imbalance between vasoconstriction and vasodilatation, which causes tissue reperfusion, cytotoxic edema, and brain injury [37].…”

Section: The Role Of Endothelial Nitric Oxide Synthase Activity In Thmentioning

confidence: 99%

Endothelial Nitric Oxide Synthase and Neurodevelopmental Disorders

Huseynova¹,

Panakhova²,

Hasanov³

et al. 2017

Nitric Oxide Synthase - Simple Enzyme-Complex Roles

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Endothelial activity relects the balance of endogenous factors regulating vasoconstriction and vasodilation. Among these factors, nitric oxide (NO) is the most important contributor to the acute regulation of vascular tone. Altered nitric oxide synthesis by the vascular endothelium plays several important roles in the pathogenesis of neonatal disease through its efects on vascular homeostasis. However, the role of NO in the pathogenesis of perinatal brain injury has not been fully investigated. The present chapter explores how NO synthesis is regulated under physiological and pathological conditions, the impact of acute and chronic hypoxia on NO synthase activity in the vascular endothelium, and the role of perinatal endothelial dysfunction in the pathogenesis of neurodevelopmental disorders later in life.

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The immune response after hypoxia-ischemia in a mouse model of preterm brain injury

Cited by 61 publications

References 68 publications

Brain-immune interactions in perinatal hypoxic-ischemic brain injury

Brain-immune interactions in perinatal hypoxic-ischemic brain injury

Chorioamnionitis, IL‐17A, and fetal origins of neurologic disease

Endothelial Nitric Oxide Synthase and Neurodevelopmental Disorders

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