质子和过敏性炎症基因的表达增加预测了儿科eosinophilic食道炎中的PPI失败
Paroma Bose1, Wenwu Zhang2, Pegah Mehrpouya-Bahrami2,3
1Department of Pediatrics, Division of Pediatric Gastroenterology, Hepatology, and Nutrition, Indiana University School of Medicine/Riley Hospital for Children, Indianapolis, IN, USA.
概括
用质子抑制剂 (PPI) 治疗埃索诺菲尔性食道炎 (EoE) 显示出不同的成功. 乳腺细胞,细胞因子和质子基因的基因表达水平较高的基因表达在儿童中预测了对PPI的不响应.
科学领域:
- 胃肠病学 胃肠病学
- 免疫学 免疫学 免疫学
- 遗传学 是一个遗传学.
背景情况:
- 质子抑制剂 (PPI) 是对性食道炎 (EoE) 的标准治疗方法.
- 然而,在儿科EoE研究中,PPI应答率存在显著差异 (23-63%).
- 预测 PPI 的响应性对于有效的 EoE 管理至关重要.
研究的目的:
- 调查食道粘膜中的特定基因表达是否可以预测儿科EOE中的PPI响应.
- 在EoE中识别PPI治疗结果的潜在生物标志物.
主要方法:
- 对新诊断的EoE儿童进行了前性研究,他们接受了8周的PPI治疗.
- 消化管活检分析基因表达使用Nanostring nCounter和免疫组织化学.
- 根据随访活检的乙氨基酸细胞计数,被归类为PPI-响应 (PPI-R) 或PPI-不响应 (PPI-NR) 的患者.
主要成果:
- 32%的EoE儿童获得了PPI-R.
- 与PPI-R EoE和对照组相比,在PPI-NR EoE中观察到较高的ATP12A,ATP4A,三酶β2 (TPSB2),CLC和IL13基因的基线表达.
- 与对照组相比,在PPI-R和PPI-NR EoE中,ATP12A染色增加.
- PPI-NR EoE显示了与巨细胞,细胞因子,质子和埃索诺菲尔相关的基因表达显著更高的基线.
结论:
- 细胞,细胞因子和质子基因基因的基线表达升高可能预测EoE中的PPI不响应.
- 一个潜在的机制涉及巨细胞激活,IL-13释放,以及质子基因 (ATP12A,ATP4A) 的上调,从而导致乙氨基的招募.
- 组织学PPI失败可能发生在这些炎症成分高度表达并且无法通过药理克服的情况下.
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