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

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

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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.
c Department of Biomedical Research , Nemours/Alfred I.duPont Hospital for Children , Wilmington , DE , USA.



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.


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.


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 (pā€‰<ā€‰.001). Similarly, HSP70 levels were significantly increased in pepsin A-positive polyp tissues than in pepsin A-negative polyp tissues (pā€‰=ā€‰.016). Furthermore, no association was found between the presence of pepsin A and HSPA5, COX-2, and CAIII mRNA expression levels.


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.


Laryngopharyngeal reflux; chronic rhinosinusitis; heat shock protein 70; pepsin A

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