Department of Pediatrics, Case Western Reserve University, 11100 Euclid Avenue, Cleveland, OH 44106, USA.
Respir Physiol Neurobiol. 2011 Sep 30;178(3):458-64. doi: 10.1016/j.resp.2011.03.003. Epub 2011 Mar 17.
Perinatal sepsis and inflammation trigger lung and brain injury in preterm infants, and associated apnea of prematurity. We hypothesized that endotoxin exposure in the immature lung would upregulate proinflammatory cytokine mRNA expression in the medulla oblongata and be associated with impaired respiratory control. Lipopolysaccharide (LPS, 0.1mg/kg) or saline was administered intratracheally to rat pups and medulla oblongatas were harvested for quantifying expression of mRNA for proinflammatory cytokines. LPS-exposure significantly increased medullary mRNA for IL-1β and IL-6, and vagotomy blunted this increase in IL-1β, but not IL-6. Whole-body flow plethysmography revealed that LPS-exposed pups had an attenuated ventilatory response to hypoxia both before and after carotid sinus nerve transection. Immunochemical expression of IL-1β within the nucleus of the solitary tract and area postrema was increased after LPS-exposure. In summary, intratracheal endotoxin-exposure in rat pups is associated with upregulation of proinflammatory cytokines in the medulla oblongata that is vagally mediated for IL-1β and associated with an impaired hypoxic ventilatory response.
围产期败血症和炎症会引发早产儿的肺部和脑部损伤，以及与之相关的早产儿呼吸暂停。我们假设，不成熟的肺部接触内毒素会导致延髓中促炎细胞因子 mRNA 表达上调，并与呼吸控制受损有关。将脂多糖（LPS，0.1mg/kg）或生理盐水气管内给药给大鼠幼仔，并收获延髓以定量测定促炎细胞因子的 mRNA 表达。LPS 暴露显著增加了延髓中 IL-1β 和 IL-6 的 mRNA，迷走神经切断术减弱了 IL-1β 的这种增加，但对 IL-6 没有影响。全身流量描记法显示，LPS 暴露的幼仔在颈动脉窦神经切断前后对缺氧的通气反应减弱。LPS 暴露后，孤束核和后极区的 IL-1β 免疫化学表达增加。总之，大鼠幼仔气管内内毒素暴露与延髓中促炎细胞因子的上调有关，这种上调与缺氧通气反应受损有关，IL-1β 则与迷走神经有关。
