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Research Article

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

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Pages 1253-1259 | Received 01 Jun 2017, Accepted 16 Jul 2017, Published online: 08 Aug 2017
 

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.

Chinese abstract

目的:探讨咽喉回流(LPR)与慢性鼻窦炎(CRS)之间的关系;探讨胃蛋白酶A对CRS中热休克蛋白70(HSP70)水平的影响。

方法:我们的研究对象是23例有鼻息肉的CRS患者(CRSwNP), 26例无鼻息肉CRS患者(CRSsNP)和9例正常对照组, 测定鼻分泌物、血浆和鼻组织中胃蛋白酶A水平, 测定鼻组织中HSP70水平, 并检测鼻组织中的胃蛋白酶原A、HSPA5、环加氧酶-2(COX-2)和碳酸酐酶III(CAIII)mRNA表达水平。

结果:CRSwNP/CRSsNP患者鼻腔分泌物中胃蛋白酶A水平明显高于对照组。与对照组相比, 胃蛋白酶A阳性鼻甲粘膜HSP70水平显著升高(p < 0.001)。类似地, 胃蛋白酶A阳性息肉组织中HSP70水平显著高于胃蛋白酶A阴性息肉组织(p = 0.016)。此外, 在胃蛋白酶A及HSPA5的存在、COX-2和CAIII mRNA表达水平之间没有发现关联。

结论:这些结果表明LPR可能通过胃蛋白酶A回流在CRS的发展中发挥作用, 并且增加的HSP70表达可能与CRS中粘膜损伤的致病机制相关。

Disclosure statement

No potential conflict of interest was reported by the authors.

Additional information

Funding

National Natural Science Foundation of China10.13039/501100001809
International Scientific and Technological Cooperation Projects of Sichuan Province
This study was funded by National Natural Science Foundation of China (No. 81170898, No. 30801280); the International Scientific and Technological Cooperation Projects of Sichuan Province (No. 2016HH0064).

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