ArticlePloS one2025
Weak acid and pepsin reflux induce laryngopharyngeal mucosal barrier injury: A rabbit-model-based study.
Article in PloS one, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- Pepsin-induced Differential IL-6 Expression in Laryngeal and Laryngopharyngeal Tissue: Non-invasive Rat Model for Laryngopharyngeal Reflux.Iranian journal of otorhinolaryngology · 2026Article
- Amprenavir Mitigates Pepsin-Induced Transcriptomic Changes in Normal and Precancerous Esophageal Cells.International journal of molecular sciences · 2025Article
- Gastroesophageal reflux-induced cough: the positive feedback loop of microaspiration and neurogenic inflammation.Therapeutic advances in respiratory diseaseReview
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8 authors.
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Abstract
objectiveUsing 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.
methodsThe 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.
resultsEight 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).
conclusionThis 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.
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