[气道神经源性炎症在胃食管反流性咳嗽中的作用]

[The role of airway neurogenic inflammation in gastro-esophageal reflux induced cough].

作者信息

Liu Chun-li, Lai Ke-fang, Chen Ru-chong, Luo Wei, Zeng Yun-xiang, Yao Wei-min, Zhong Nan-shan

机构信息

Guangzhou Institute of Respiratory Disease, First Affiliated Hospital of Guangzhou Medical College, Guangzhou 510120, China.

出版信息

Zhonghua Jie He He Hu Xi Za Zhi. 2005 Aug;28(8):520-4.

PMID:16207397

Abstract

OBJECTIVE

To investigate the role of airway neurogenic inflammation in the pathogenesis of gastro-esophageal reflux induced cough (GERC).

METHODS

Sputum was induced by hypertonic saline aerosol inhalation in 20 patients with GERC (GERC group), 10 healthy subjects (normal control group) and 8 patients with chronic cough due to other causes but complicated with gastro-esophageal reflux diseases (GERD, GERD group). Airway mucosal biopsy was performed in 6 patients with GERC and 4 patients with GERD using flexible fiberoptic bronchoscopy. The expression of substance P (SP), neurokinin 1 receptor and neurokinin A (NKA) in sputum cells and airway mucosa were detected by immunohistochemistry, and was assessed semi-quantitatively. SP, NKA, and NKB in the supernatant of induced sputum were measured with enzyme linked immunosorbent assay. Calcitonin gene-related peptide (CGRP) was measured with radioimmunoassay.

RESULTS

The concentration of SP in the supernatant of induced sputum was significantly higher in GERC group [(266 +/- 207) ng/L] than those in normal control group [(143 +/- 36) ng/L, P < 0.05] and GERD group [(130 +/- 11) ng/L, P < 0.05], and the sputum supernatant concentration of CGRP in GERC group [(180 +/- 83) ng/L] was significantly higher than those in normal control group [(105 +/- 64) ng/L, P < 0.01] and GERD group [(89 +/- 16) ng/L, P < 0.01]. The expression of SP, NK-1 receptor and NKA in induced sputum cells in GERC group were significantly higher than those in normal control group (P < 0.01, < 0.05, < 0.05) and GERD group (all P < 0.05); Expressions of SP in airway mucosa was significantly higher in GERC group than in GERD group (P < 0.01). After treatment, the concentration of CGRP in the supernatant of sputum in GERC patients was significantly lower than that before treatment (P < 0.05); the expression of SP, NK-1 and NKA in the induced sputum cells were significantly lower than that before treatment (P < 0.01, P < 0.01 or P < 0.05).

CONCLUSION

There is airway neurogenic inflammation in GERC patients, which maybe closely related to the development of GERC.

摘要

目的

探讨气道神经源性炎症在胃食管反流性咳嗽（GERC）发病机制中的作用。

方法

对20例GERC患者（GERC组）、10例健康受试者（正常对照组）和8例因其他原因导致慢性咳嗽但合并胃食管反流病（GERD，GERD组）的患者，通过雾化吸入高渗盐水诱导痰液。对6例GERC患者和4例GERD患者采用可弯曲纤维支气管镜进行气道黏膜活检。采用免疫组织化学法检测痰液细胞和气道黏膜中P物质（SP）、神经激肽1受体和神经激肽A（NKA）的表达，并进行半定量评估。采用酶联免疫吸附测定法检测诱导痰液上清液中的SP、NKA和神经激肽B（NKB）。采用放射免疫测定法检测降钙素基因相关肽（CGRP）。

结果

GERC组诱导痰液上清液中SP浓度[（266±207）ng/L]显著高于正常对照组[（143±36）ng/L，P<0.05]和GERD组[（130±1）ng/L，P<0.05]；GERC组痰液上清液中CGRP浓度[（180±83）ng/L]显著高于正常对照组[（105±64）ng/L，P<0.01]和GERD组[（89±16）ng/L，P<0.01]。GERC组诱导痰液细胞中SP、NK-1受体和NKA的表达显著高于正常对照组（P<0.01、<0.05、<0.05）和GERD组（均P<0.05）；GERC组气道黏膜中SP的表达显著高于GERD组（P<0.01）。治疗后，GERC患者痰液上清液中CGRP浓度显著低于治疗前（P<0.05）；诱导痰液细胞中SP、NK-1和NKA的表达显著低于治疗前（P<0.01、P<0.01或P<0.05）。