Department of Medicine, University of Michigan Medical School, Ann Arbor, Michigan 48109, USA.
Am J Physiol Gastrointest Liver Physiol. 2011 Dec;301(6):G1052-8. doi: 10.1152/ajpgi.00015.2011. Epub 2011 Sep 29.
Eosinophilic esophagitis is characterized by increased infiltration and degranulation of eosinophils in the esophagus. Whether eosinophil-derived cationic proteins regulate esophageal sensory nerve function is still unknown. Using synthetic cationic protein to investigate such effect, we performed extracellular recordings from vagal nodose or jugular neurons in ex vivo esophageal-vagal preparations with intact nerve endings in the esophagus. Nerve excitabilities were determined by comparing action potentials evoked by esophageal distensions before and after perfusion of synthetic cationic protein poly-L-lysine (PLL) with or without pretreatment with poly-L-glutamic acid (PLGA), which neutralized cationic charges of PLL. Perfusion with PLL did not evoke action potentials in esophageal nodose C fibers but increased their responses to esophageal distension. This potentiation effect lasted for 30 min after washing out of PLL. Pretreatment with PLGA significantly inhibited PLL-induced mechanohyperexcitability of esophageal nodose C fibers. In esophageal nodose Aδ fibers, perfusion with PLL did not evoke action potentials. In contrast to nodose C fibers, both the spontaneous discharges and the responses to esophageal distension in nodose Aδ fibers were decreased by perfusion with PLL, which can be restored after washing out PLL for 30-60 min. Pretreatment with PLGA attenuated PLL-induced decrease in spontaneous discharge and mechanoexcitability of esophageal nodose Aδ fibers. In esophageal jugular C fibers, PLL neither evoked action potentials nor changed their responses to esophageal distension. Collectively, these data demonstrated that synthetic cationic protein did not evoke action potential discharges of esophageal vagal afferents but had distinctive sensitization effects on their responses to esophageal distension.
嗜酸性食管炎的特征是食管中嗜酸性粒细胞的浸润和脱颗粒增加。嗜酸性粒细胞衍生的阳离子蛋白是否调节食管感觉神经功能尚不清楚。我们使用合成阳离子蛋白来研究这种作用,在离体食管-迷走神经制备物中,从迷走神经结或颈神经元进行细胞外记录,该制备物保留了完整的食管神经末梢。通过比较在灌注合成阳离子蛋白聚-L-赖氨酸(PLL)前后,通过或不预先用聚-L-谷氨酸(PLGA)处理,刺激食管膨胀诱发的动作电位来确定神经兴奋性,PLGA 中和 PLL 的阳离子电荷。PLL 灌注不会在食管迷走神经 C 纤维中诱发动作电位,但增加了它们对食管膨胀的反应。这种增强作用在 PLL 冲洗后持续 30 分钟。PLGA 的预处理显著抑制了 PLL 诱导的食管迷走神经 C 纤维的机械超兴奋性。在食管迷走神经 Aδ 纤维中,PLL 灌注不会诱发动作电位。与迷走神经 C 纤维相反,PLL 灌注既降低了迷走神经 Aδ 纤维的自发性放电,也降低了它们对食管膨胀的反应,这种作用在 PLL 冲洗 30-60 分钟后可以恢复。PLGA 的预处理减轻了 PLL 诱导的食管迷走神经 Aδ 纤维自发性放电和机械兴奋性的降低。在食管颈 C 纤维中,PLL 既不诱发动作电位,也不改变它们对食管膨胀的反应。综上所述,这些数据表明,合成阳离子蛋白不会诱发食管迷走传入神经的动作电位,但对其对食管膨胀的反应有独特的敏化作用。