Expression and significance of interleukin-17 and interleukin-22 in the serum and the lower esophageal sphincter of patients with achalasia

Expression and significance of interleukin-17 and interleukin-22 in the serum and the lower esophageal sphincter of patients with achalasia
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DOI:
10.4103/sjg.sjg_562_17
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发表时间:
2018-07-01
影响因子:
2.7
通讯作者:
Zhao, Dongqiang
Zhao, Dongqiang
中科院分区:
医学4区
文献类型:
--
作者:
Wang, Zeyu;Zhang, Jun;Zhao, Dongqiang

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目的:研究白介素17和白介素22在健康体检者和失弛缓症患者血清和下食道括约肌中的表达,以进一步了解失弛缓症的发病机制。对所有研究对象的静脉血样本进行评估,用酶联免疫吸附试验检测血清中IL-17和IL-22的表达。结果:与对照组相比,AC患者血清和LES中IL-17和IL-22的表达显著增加,且呈正相关。结论:AC患者血清和LES中IL-17和IL-22的表达均显著高于对照组,且呈正相关。结论:AC患者血清和LES中IL-17和IL-22的表达均上调,提示IL-17和IL-22均参与了AC的发病过程。AC可能是一种免疫介导性炎症性疾病。
Background/Aim: We studied the expression of interleukin-17 and interleukin-22 in the serum and the lower esophageal sphincter (LES) in healthy individuals and in patients diagnosed with achalasia (AC) to gain a better understanding of the etiopathogenesis of AC.Patients and Methods: Our study comprised 14 randomly selected patients with AC who underwent peroral endoscopic myotomy and 14 randomly selected healthy individuals who served as controls. Venous blood samples were evaluated in all study subjects to detect the expression of interleukin-17 and interleukin-22 in the serum using an enzyme-linked immunosorbent assay. Immunohistochemistry studies were performed to evaluate LES myofilaments obtained from both groups, as well as from 12 patients diagnosed with a subendothelial non-invasive tumor and who had undergone submucosal tunneling endoscopic resection, to assess the expression of interleukin-17 and interleukin-22 in LES myofilaments.Results: Compared with that in the control group, the expression of interleukin-17 and interleukin-22 in the serum and LES, in patients with AC, was significantly increased and was positively correlated.Conclusion: Interleukin-17 and interleukin-22 are upregulated in the serum and LES in patients with AC, suggesting that both interleukin-17 and interleukin-22 are involved in the pathogenesis of AC, and that AC may be an immune-mediated inflammatory disease.