Dataset Information

Extra-Esophageal Pepsin from Stomach Refluxate Promoted Tonsil Hypertrophy.

ABSTRACT:

Background

Gastroesophageal reflux is associated with numerous pathologic conditions of the upper aerodigestive tract. Gastric pepsin within reflux contributes to immunologic reactions in the tonsil. In this study, we aimed to find the relationships between pepsin and tonsillar hypertrophy.

Methods and finding

We explored the notion whether tonsillar hypertrophy was due to pepsin-mediated gastric reflux in tonsil hypertrophy. Fifty-four children with tonsil hypertrophy and 30 adults with tonsillitis were recruited before surgical treatment. Blood and tonsil tissues from each patient were harvested for analysis of changes in lymphocyte and macrophage numbers coupled with histological and biochemical analysis. Pepsin was expressed at different levels in tonsil tissues from each tonsillar hypertrophy. Pepsin-positive cells were found in the crypt epithelium, surrounding the lymphoid follicle with developing fibrosis, and also surrounding the lymphoid follicle that faced the crypt. And also, pepsin staining was well correlated with damaged tonsillar squamous epithelium and TGF-β1 and iNOS expression in the tonsil section. In addition, pepsin and TGF-β1-positive cells were co-localized with CD68-positive cells in the crypt and surrounding germinal centers. In comparison of macrophage responsiveness to pepsin, peripheral blood mononuclear cells (PBMNCs) were noticeably larger in the presence of activated pepsin in the child group. Furthermore, CD11c and CD163-positive cells were significantly increased by activated pepsin. However, this was not seen for the culture of PBMNCs from the adult group.

Conclusions

The lymphocytes and monocytes are in a highly proliferative state in the tonsillar hypertrophy and associated with increased expression of pro-inflammatory factors as a result of exposure to stomach reflux pepsin.

SUBMITTER: Kim JH

PROVIDER: S-EPMC4825923 | biostudies-literature | 2016

REPOSITORIES: biostudies-literature

ACCESS DATA

Publications

Extra-Esophageal Pepsin from Stomach Refluxate Promoted Tonsil Hypertrophy.

Kim Jin Hyun JH Jeong Han-Sin HS Kim Kyung Mi KM Lee Ye Jin YJ Jung Myeong Hee MH Park Jung Je JJ Kim Jin Pyeong JP Woo Seung Hoon SH

PloS one 20160408 4

<h4>Background</h4>Gastroesophageal reflux is associated with numerous pathologic conditions of the upper aerodigestive tract. Gastric pepsin within reflux contributes to immunologic reactions in the tonsil. In this study, we aimed to find the relationships between pepsin and tonsillar hypertrophy.<h4>Methods and finding</h4>We explored the notion whether tonsillar hypertrophy was due to pepsin-mediated gastric reflux in tonsil hypertrophy. Fifty-four children with tonsil hypertrophy and 30 adul ...[more]

PMID: 27058240

Similar Datasets

Project description:Background: Gastroesophageal reflux disease (GERD) is a chronic condition linked to inflammatory and cancerous alterations in esophageal epithelium. Despite the widespread use of acid suppressing proton pump inhibitors (PPIs), the incidence of esophageal adenocarcinoma (EAC) keeps increasing, underscoring the possible importance of nonacidic reflux components like pepsin in cancer development. Pepsin, a therapeutic target for GERD, has been associated with epithelial damage and metaplasia. Methods: The goal of this study was to investigate the effect of pepsin, at a transcriptional level, and to assess the potential therapeutic value of amprenavir, as a pepsin inhibitor, in vitro. Human esophageal cell lines, immortalized from normal (Het-1A) and Barrett’s esophagus (BAR-T), were exposed to pH 7.0 buffer containing pepsin and/or amprenavir for 1 hour (n=3). RNA-seq was conducted to detect differentially expressed genes (DEGs) with FDR ≤ 0.05 and |log2 fold change| ≥ 0.375, and Ingenuity Pathway Analysis (IPA) was performed to identify the top significantly biological pathways. Results: Pepsin exposure caused notable transcriptomic alterations in both Het-1A and BAR-T cells, specifically impacting mitochondrial function, oxidative phosphorylation, and pathways associated with epithelial integrity, cell signaling, and inflammatory responses. Amprenavir alleviated several of these effects, indicating a protective function in epithelial impairment resulting from peptic injury. Of interest, Het-1A and BAR-T cells demonstrated different reactions to pepsin treatment; BAR-T cells revealed more pronounced changes in pathways associated with wound healing, chronic epithelial formation, and repair, whereas Het-1A cells showed more substantial alterations in systemic damage and mitochondrial pathways. Conclusion: The results of this study underscore the detrimental impact of pepsin on esophageal epithelial cells despite PPI therapy and highlight amprenavir as a promising therapeutic option to mitigate pepsin-induced epithelial injury. Further research to validate these in vitro findings is warranted to assess the efficacy of amprenavir for GERD-related damage and carcinogenesis.

Dataset Information

Extra-Esophageal Pepsin from Stomach Refluxate Promoted Tonsil Hypertrophy.

Background

Methods and finding

Conclusions

Publications

Extra-Esophageal Pepsin from Stomach Refluxate Promoted Tonsil Hypertrophy.

Similar Datasets

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