Hou Chenjie, Zhou Liqun, Zheng Yujin, Chen Ting, Hu Renyou, Zheng Jingyi, Liu Chaofeng, Liu Yaqi
Department of Otorhinolaryngology, Fujian Provincial Hospital, Fuzhou, Fujian, China.
Department of Otorhinolaryngology, Shengli Clinical Medical College of Fujian Medical University, Fuzhou, Fujian, China.
PLoS One. 2025 Jan 24;20(1):e0315083. doi: 10.1371/journal.pone.0315083. eCollection 2025.
Using rabbit models, this study simulated the laryngopharynx's response to the synergistic effects of various acidic reflux environments and pepsin to investigate the response mechanism underlying weak acid reflux and pepsin in the mucosal barrier injury of laryngopharyngeal reflux.
The rabbits were divided into six groups, and the original larynx was recorded for each group. During the study period, rabbits were sprayed with different doses of acid and pepsin solutions and monitored for hypopharyngeal mucosal transient impedance before and after modeling. After the experiment, laryngeal mucosal tissues were collected, observed using hematoxylin and eosin staining, and assessed for E-cadherin expression. The width of the intercellular space and lanthanum staining penetrating the intercellular space were also observed using electron microscopy.
Eight weeks post-modeling, evidence of laryngopharyngeal mucosa inflammatory responses was observed in each group. Downregulation of E-cadherin expression significantly positively correlated with acid strength (p < 0.05). The pepsin and acid intervention groups showed a significantly widened space between mucosal epithelial cells in the posterior ring area (p < 0.05). Meanwhile, in the experimental group, a large amount of stained lanthanum penetrated the intercellular spaces; however, no significant difference was observed in the mucosal impedance (MI).
This study demonstrated that acid, weak acid, and pepsin could damage the laryngeal mucosal barrier; pepsin was an independent factor associated with tissue damage; the downregulation of hypopharyngeal cadherin was associated with acid-intensity exposure. Transient LP-MI cannot be applied directly.
本研究采用兔模型，模拟下咽对各种酸性反流环境和胃蛋白酶协同作用的反应，以探讨弱酸反流和胃蛋白酶在喉咽反流黏膜屏障损伤中的反应机制。
将兔分为六组，记录每组兔的原始喉部情况。在研究期间，给兔喷洒不同剂量的酸和胃蛋白酶溶液，并在建模前后监测下咽黏膜瞬时阻抗。实验结束后，收集喉黏膜组织，采用苏木精-伊红染色观察，并评估E-钙黏蛋白的表达。同时，利用电子显微镜观察细胞间隙宽度以及镧染色穿透细胞间隙的情况。
建模8周后，每组均观察到喉咽黏膜炎症反应的证据。E-钙黏蛋白表达下调与酸强度呈显著正相关（p<0.05）。胃蛋白酶和酸干预组在后环区黏膜上皮细胞之间的间隙明显增宽（p<0.05）。同时，实验组有大量镧染色穿透细胞间隙；然而，黏膜阻抗（MI）未见显著差异。
本研究表明，酸、弱酸和胃蛋白酶均可损伤喉黏膜屏障；胃蛋白酶是与组织损伤相关的独立因素；下咽钙黏蛋白下调与酸强度暴露有关。不能直接应用瞬时喉咽-黏膜阻抗。
