Department of Pediatrics, Division of Neonatology, Rainbow Babies & Children's Hospital, Cleveland, OH 44106, USA.
Respir Physiol Neurobiol. 2013 Aug 1;188(1):21-8. doi: 10.1016/j.resp.2013.04.022. Epub 2013 May 3.
Perinatal inflammation is associated with respiratory morbidity. Immune modulation of brainstem respiratory control centers may provide a link for this pathobiology. We exposed 11-day old rats to intratracheal lipopolysaccharide (LPS, 0.5 μg/g) to test the hypothesis that intrapulmonary inflammation increases expression of the proinflammatory cytokine IL-1β within respiratory-related brainstem regions. Intratracheal LPS resulted in a 32% increase in IL-1β protein expression in the medulla oblongata. In situ hybridization showed increased intensity of IL-1β mRNA but no change in neuronal numbers. Co-localization experiments showed that hypoglossal neurons express IL-1β mRNA and immunostaining showed a 43% increase in IL-1β protein-expressing cells after LPS exposure. LPS treatment also significantly increased microglial cell numbers though they did not express IL-1β mRNA. LPS-induced brainstem expression of neuronal IL-1β mRNA and protein may have implications for our understanding of the vulnerability of neonatal respiratory control in response to a peripheral proinflammatory stimulus.
围产期炎症与呼吸发病率有关。脑干呼吸控制中心的免疫调节可能为此病理生物学提供了联系。我们将 11 天大的大鼠暴露于气管内脂多糖（LPS，0.5μg/g）中，以检验以下假设：肺内炎症会增加与呼吸相关的脑干区域中促炎细胞因子 IL-1β的表达。气管内 LPS 导致延髓中 IL-1β蛋白表达增加 32%。原位杂交显示 IL-1β mRNA 的强度增加，但神经元数量没有变化。共定位实验表明舌下神经神经元表达 IL-1β mRNA，免疫染色显示 LPS 暴露后表达 IL-1β 蛋白的细胞增加了 43%。LPS 处理还显著增加了小胶质细胞数量，尽管它们不表达 IL-1β mRNA。LPS 诱导的脑干神经元 IL-1β mRNA 和蛋白表达可能对我们理解新生儿呼吸控制对外周促炎刺激的易感性具有重要意义。
