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肺内脂多糖暴露可上调新生儿脑干细胞因子的表达。

Intrapulmonary lipopolysaccharide exposure upregulates cytokine expression in the neonatal brainstem.

机构信息

Rainbow Babies & Children's Hospital, University Hospitals Case Medical Center, Case Western Reserve University, Cleveland, OH 44106-6010, USA.

出版信息

Acta Paediatr. 2012 May;101(5):466-71. doi: 10.1111/j.1651-2227.2011.02564.x. Epub 2012 Jan 11.

Abstract

UNLABELLED

Perinatal inflammation and neonatal sepsis trigger lung and brain injury. We hypothesized that endotoxin exposure in the immature lung upregulates proinflammatory cytokine expression in the brainstem and impairs respiratory control. Lipopolysaccharide (LPS) or saline was administered intratracheally to vagal intact or denervated rat pups. LPS increased brainstem IL-1β and vagotomy blunted this response. There was an attenuated ventilatory response to hypoxia and increased brainstem IL-1β expression after LPS.

CONCLUSION

Intratracheal endotoxin exposure in rat pups is associated with upregulation of IL-1β in the brainstem that is vagally mediated and associated with an impaired hypoxic ventilatory response.

摘要

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围产期炎症和新生儿败血症会引发肺部和脑部损伤。我们假设,不成熟肺部的内毒素暴露会在上脑干上调促炎细胞因子的表达,并损害呼吸控制。将脂多糖(LPS)或生理盐水通过气管内滴注到迷走神经完整或去神经的大鼠幼仔中。LPS 增加了脑干中的 IL-1β,而迷走神经切断术则减弱了这种反应。LPS 后,对缺氧的通气反应减弱,并且脑干中的 IL-1β表达增加。

结论

在大鼠幼仔中经气管内内毒素暴露与脑干中 IL-1β的上调有关,该上调是通过迷走神经介导的,并与缺氧通气反应受损有关。

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