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Background <p>Laryngopharyngeal reflux (LPR) involves microbiota dysbiosis and changes in the salivary pre-epithelial barrier. However, the interaction between these factors, which impact gastroesophageal reflux disease (GERD), remains unknown. Herein, we conducted a comparative cross-sectional study enrolling 36 individuals with LPR, diagnosed by Diagnostic Potential of Hydrogen Monitoring System (Dx-pH monitoring), and 39 healthy controls. The salivary flow and key salivary pre-epithelial barrier factors, epidermal growth factor (EGF), transforming growth factor-alpha (TGF-α), mucin 5B (MUC5B), mucin 7 (MUC7), secretory immunoglobulin A (SIgA), were assessed along with microbiome examination.</p> Results <p>LPR individuals exhibited a reduced salivary flow (<i>P</i> = 0.008) and salivary secretion of EGF (<i>P</i> = 0.029), TGF-α (<i>P</i> = 0.028) and MUC5B (<i>P</i> = 0.010) when compared to those of healthy controls. Additionally, compared with those in the control group, the 5-minute secretory quantity of MUC7 (<i>P</i> = 0.086) and SIgA (<i>P</i> = 0.255) were also lower in the LPR patient group, but these differences were not statistically significant (<i>P</i> &gt; 0.05). Distinct bacterial communities were identified in the LPR group, with a significant increase in acid-resistant bacteria, including <i>Prevotella</i> and <i>Veillonella</i>. Additionally, the abundance of <i>Prevotella</i> (γ= -0.639, <i>P</i> = 0.002) was significantly negatively correlated with EGF concentration in LPR patients.</p> Conclusion <p>Our findings demonstrate that LPR is associated with both distinct salivary microbial profiles and disruption of the pre-epithelial mucosal barrier constituents. These observations support a potential role for salivary microbiota dysbiosis in the pathogenesis of LPR, highlighting a novel interconnection between microbial community perturbations and mucosal barrier dysfunction in this disease.</p> Level of evidence： <p>4</p> Trial registration <p>No. ChiCTR2400091947. Registered on November 6,2024 retrospectively.</p>

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Association of the microbiome with pre-epithelial barrier impairment in individuals with laryngopharyngeal reflux

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年12月10日

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  • Xiaohuan Cui,
  • Xinxin Bi,
  • Linxi Zhou,
  • Xingwang Jiang,
  • Yanping Zhang,
  • Lina Li,
  • Xiaohang Jing,
  • Shuang Guo

摘要

Background

Laryngopharyngeal reflux (LPR) involves microbiota dysbiosis and changes in the salivary pre-epithelial barrier. However, the interaction between these factors, which impact gastroesophageal reflux disease (GERD), remains unknown. Herein, we conducted a comparative cross-sectional study enrolling 36 individuals with LPR, diagnosed by Diagnostic Potential of Hydrogen Monitoring System (Dx-pH monitoring), and 39 healthy controls. The salivary flow and key salivary pre-epithelial barrier factors, epidermal growth factor (EGF), transforming growth factor-alpha (TGF-α), mucin 5B (MUC5B), mucin 7 (MUC7), secretory immunoglobulin A (SIgA), were assessed along with microbiome examination.

Results

LPR individuals exhibited a reduced salivary flow (P = 0.008) and salivary secretion of EGF (P = 0.029), TGF-α (P = 0.028) and MUC5B (P = 0.010) when compared to those of healthy controls. Additionally, compared with those in the control group, the 5-minute secretory quantity of MUC7 (P = 0.086) and SIgA (P = 0.255) were also lower in the LPR patient group, but these differences were not statistically significant (P > 0.05). Distinct bacterial communities were identified in the LPR group, with a significant increase in acid-resistant bacteria, including Prevotella and Veillonella. Additionally, the abundance of Prevotella (γ= -0.639, P = 0.002) was significantly negatively correlated with EGF concentration in LPR patients.

Conclusion

Our findings demonstrate that LPR is associated with both distinct salivary microbial profiles and disruption of the pre-epithelial mucosal barrier constituents. These observations support a potential role for salivary microbiota dysbiosis in the pathogenesis of LPR, highlighting a novel interconnection between microbial community perturbations and mucosal barrier dysfunction in this disease.

Level of evidence：

4

Trial registration

No. ChiCTR2400091947. Registered on November 6,2024 retrospectively.