Abstract
BackgroundGastroesophageal 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 findingWe 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.ConclusionsThe 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.
Highlights
Tonsil hypertrophy is currently the most common reason for tonsillectomy
Immunoblot data showed that pepsin protein was expressed as a single band from extracts of both the tonsil of patients with tonsil hypertrophy
No pepsin staining was observed in other tissues including tumor, lymph node (LN), thyroid (Thy), parotid gland (Parotid g.), salivary gland (SG) (Fig 1A)
Summary
Enlargement of the tonsils occurs due to an absolute increase in the total number of lymphocytes in the tissue and resulting in an increase in tissue volume.[1, 2] The precise mechanism by which lymphocyte stimulation and proliferation occurs has yet to be determined. Previous attempts at identifying the pathophysiologic mechanisms have focused on microbiological and immunologic changes in enlarged tonsils. Many studies have reported a possible role of bacterial organisms in the pathogenesis of tonsil hypertrophy.[3,4,5] an increase in the absolute number of lymphocytes within the tonsils without a clinical infection was previously shown[2], and the specific antigens responsible for these changes have not been identified. We aimed to find the relationships between pepsin and tonsillar hypertrophy
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