胃蛋白酶A对慢性鼻窦炎伴喉咽反流患者热休克蛋白70反应的影响。

Effects of pepsin A on heat shock protein 70 response in laryngopharyngeal reflux patients with chronic rhinosinusitis.

作者信息

Wang Jing, Yu Zhao, Ren Jianjun, Xu Yang, Zhang Yuke, Lei Lei, Zheng Yongbo, Huang Ligao, He Zhaoping

机构信息

a Department of Oto-Rhino-Laryngology , West China Hospital, West China Medical School, Sichuan University , Chengdu , Sichuan , China.

b Department of Otolaryngology , Chengdu Renpin Otorhinolaryngological Hospital , Chengdu , Sichuan , China.

出版信息

Acta Otolaryngol. 2017 Dec;137(12):1253-1259. doi: 10.1080/00016489.2017.1360515. Epub 2017 Aug 8.

Abstract

OBJECTIVES

We investigated the relationship between laryngopharyngeal reflux (LPR) and chronic rhinosinusitis (CRS), and explored the effects of pepsin A on the level of heat shock protein 70 (HSP70) in CRS.

METHODS

We included 23 CRS patients with nasal polyps (CRSwNP), 26 CRS patients without nasal polyps (CRSsNP) and nine normal controls to measure pepsin A levels in nasal secretions, blood plasma and nasal tissues, to measure HSP70 levels in nasal tissues, and to detect pepsinogen A, HSPA5, cyclo-oxygenase-2 (COX-2), and carbonic anhydrase III (CAIII) mRNA expression levels in nasal tissues.

RESULTS

Pepsin A levels in nasal secretions were significantly higher in CRSwNP/CRSsNP patients than in controls. HSP70 levels were significantly increased in pepsin A-positive turbinate mucosa compared to controls (p < .001). Similarly, HSP70 levels were significantly increased in pepsin A-positive polyp tissues than in pepsin A-negative polyp tissues (p = .016). Furthermore, no association was found between the presence of pepsin A and HSPA5, COX-2, and CAIII mRNA expression levels.

CONCLUSIONS

These results suggest that LPR may play a role in the development of CRS through pepsin A reflux, and increased HSP70 expression may be associated with the pathogenic mechanism of mucosal injury in CRS.

摘要

目的

我们研究了喉咽反流(LPR)与慢性鼻-鼻窦炎(CRS)之间的关系,并探讨了胃蛋白酶A对CRS中热休克蛋白70(HSP70)水平的影响。

方法

我们纳入了23例伴有鼻息肉的CRS患者(CRSwNP)、26例不伴有鼻息肉的CRS患者(CRSsNP)和9名正常对照者,以测量鼻分泌物、血浆和鼻组织中的胃蛋白酶A水平,测量鼻组织中的HSP70水平,并检测鼻组织中胃蛋白酶原A、HSPA5、环氧化酶-2(COX-2)和碳酸酐酶III(CAIII)的mRNA表达水平。

结果

CRSwNP/CRSsNP患者鼻分泌物中的胃蛋白酶A水平显著高于对照组。与对照组相比,胃蛋白酶A阳性的鼻甲黏膜中HSP70水平显著升高(p <.001)。同样,胃蛋白酶A阳性的息肉组织中HSP70水平显著高于胃蛋白酶A阴性的息肉组织(p = 0.016)。此外,未发现胃蛋白酶A的存在与HSPA5、COX-2和CAIII的mRNA表达水平之间存在关联。

结论

这些结果表明,LPR可能通过胃蛋白酶A反流在CRS的发生发展中起作用,HSP70表达增加可能与CRS中黏膜损伤的发病机制有关。

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