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目的探讨气道神经源性炎症在胃食管反流性咳嗽(GERC)发病中的作用。方法20例GERC患者(GERC组),与10名正常人(正常对照组)和8例其他病因咳嗽伴有胃食管反流(GERD)患者(GERD组)分别作对比分析,观察GERC患者治疗前、后气道黏膜与分泌物中神经肽的变化。用酶联免疫吸附测定(ELISA)法测定痰上清液P物质(SP)、神经肽A(NKA)、神经肽B(NKB)的含量;用放射免疫法测定痰上清液降钙素基因相关肽(CGRP)的浓度。用免疫组化法检测气道黏膜、诱导痰细胞SP、NKA及SP受体(NK1)的表达,结果用半定量病理学方法表示。结果GERC组患者痰上清液SP、CGRP含量[(266±207)ng/L、(180±83)ng/L]显著高于正常对照组[(143±36)ng/L、(105±64)ng/L,P分别<0.05、<0.01]和GERD组[(130±11)ng/L、(89±16)ng/L,P分别<0.05、<0.01],NKA、NKB的含量各组间比较差异无统计学意义(P均>0.05);GERC组痰细胞SP、NK1和NKA的表达显著高于正常对照组(P分别<0.01、<0.05,<0.05)和GERD组(P均<0.05);GERC组气道黏膜SP的表达也显著高于GERD组(P<0.01)。治疗后,诱导痰细胞SP、NK1、NKA的表达较治疗前显著降低(P<0.01,<0.01或<0.05),痰上清液CGRP的含量也较治疗前显著降低(P<0.05)。结论GERC患者气道存在明显的神经源性炎症,治疗后神经肽趋于正常,提示神经源性炎症与GERC的发病密切相关。
Objective To investigate the role of airway neurogenic inflammation in the pathogenesis of gastroesophageal reflux cough (GERC). Methods Twenty patients with GERC (GERC group), 10 normal subjects (normal control group) and 8 patients with other etiology of cough with gastroesophageal reflux (GERD) (GERD group) were analyzed respectively. Before treatment , Post-airway mucosa and secretion of neuropeptides changes. The contents of substance P (SP), neuropeptide A (NKA) and neuropeptide B (NKB) in sputum supernatant were determined by enzyme linked immunosorbent assay (ELISA). The calcitonin gene Concentration of related peptide (CGRP). The expression of SP, NKA and SP receptor (NK1) in sputum were detected by immunohistochemistry in airway mucosa, and the results were expressed by semi-quantitative pathology. Results The levels of SP and CGRP in the sputum supernatant of patients with GERC were significantly higher than those of the normal controls [(266 ± 207) ng / L, (180 ± 83) ng / L, [(143 ± 36) (P <0.05, <0.01), and the levels of NKA and NKB in the GERD group [(130 ± 11) ng / L, The expression of SP, NK1 and NKA in sputum cells in GERC group were significantly higher than those in normal control group (P <0.01, <0.05, <0.05) and in GERD group (P <0.05, All <0.05). The expression of SP in airway mucosa of GERC group was also significantly higher than that of GERD group (P <0.01). After treatment, the expression of SP, NK1 and NKA in sputum cells decreased significantly (P <0.01, <0.01 or <0.05), and the content of CGRP in sputum supernatant was significantly lower than that before treatment (P <0.05). Conclusions There is obvious neurogenic inflammation in the airway of GERC patients. The neuropeptides tend to be normal after treatment, suggesting that neurogenic inflammation is closely related to the pathogenesis of GERC.