Dataset Information

Effects of pepsin and pepstatin on reflux tonsil hypertrophy in vitro.

ABSTRACT: There is evidence that pepsin can aggravate tonsil hypertrophy. Pepstatin is a potent inhibitor of pepsin activity and could protect patients against reflux tonsil hypertrophy by inhibiting pepsin. We examined the effects of pepstatin on the development of tonsil hypertrophy to investigate pepsin's role in the pathogenesis of tonsil lesions. We investigated whether pepstatin suppresses pepsin-mediated lymphocyte proliferation in tonsil hypertrophy. Forty-nine children with tonsil hypertrophy and twenty-two adults with tonsillitis were recruited to the study prior to surgery. Tonsil tissue from each patient was harvested and assessed for changes in the number of lymphocytes and macrophages in the presence of pepsin and pepstatin. We found that the proportions of CD4- and CD14-positive cells were significantly lower (p < 0.05), but that the proportions of CD19- and CD68-positive cells were significantly higher (p < 0.05), in children than in adults. There were significantly more CD4-positive cells after pepsin treatment, but these numbers were reduced by pepstatin. The levels of both interleukin-2 (IL-2) and interferon gamma (IFN-?) increased significantly in response to pepsin, but were reduced when pepsin was inhibited by pepstatin. The level of IL-10 is reduced in pepsin-treated CD4 cells and the level is restored by pepstatin. IL-2 blocking reduced the increased CD4 cell number by pepsin. But, an additive or a synergic effect is not founded in combined with IL-2 blocking and pepstatin. Pepsin-positive cells did not co-localize with CD20 and CD45 cells, but they were found surrounding CD20- and CD45-positive hypertrophic tonsil cells. Pepsin-positive cells co-localized with CD68-positive cells. It is probable that pepsin from extraesophageal reflux aggravates tonsil hypertrophy and pepstatin exerts a protective effect by inhibiting pepsin activity.

SUBMITTER: Kim JH

PROVIDER: S-EPMC6224077 | biostudies-literature | 2018

REPOSITORIES: biostudies-literature

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Effects of pepsin and pepstatin on reflux tonsil hypertrophy in vitro.

Kim Jin Hyun JH Jang Si Jung SJ Yun Jeong Won JW Jung Myeong Hee MH Woo Seung Hoon SH

PloS one 20181108 11

There is evidence that pepsin can aggravate tonsil hypertrophy. Pepstatin is a potent inhibitor of pepsin activity and could protect patients against reflux tonsil hypertrophy by inhibiting pepsin. We examined the effects of pepstatin on the development of tonsil hypertrophy to investigate pepsin's role in the pathogenesis of tonsil lesions. We investigated whether pepstatin suppresses pepsin-mediated lymphocyte proliferation in tonsil hypertrophy. Forty-nine children with tonsil hypertrophy and ...[more]

PMID: 30408092

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Project description:OBJECTIVE:Recently, a 24-h impedance was used to detect laryngopharyngeal reflux (LPR). However, not every case of LPR is pathological. Thus, pathological pharyngeal impedance values need to be clearly established to diagnose pathological LPR. The aim of our study was to establish pathological 24-h pharyngoesophageal impedance/pH values for the diagnosis of LPR. METHODS:The study was conducted in a tertiary care setting. A total of 30 patients who were referred to microlaryngoscopy for a laryngeal pathology that might be caused by LPR were included in this prospective study. All patients were off proton-pump inhibitor therapy. The 24-h pharyngoesophageal impedance-pH monitoring was performed 1 day before surgery. A biopsy of laryngeal tissue was obtained during microlaryngoscopy and was analyzed by immunohistochemistry to detect pepsin. The patients were divided into two groups: pepsin negative and pepsin positive (which indicated pathological LPR). The results of 24-h multichannel intraluminal impedance-dual-channel pH monitoring were compared between the groups. The number of LPR episodes in the pepsin-positive group was analyzed to establish a cutoff value for pathological LPR. RESULTS:There were 18 participants in the pepsin-negative group and 12 in the pepsin-positive group. The median total pharyngeal refluxes detected were two (0-5) in the pepsin-negative group and 14 (6-39) in the pepsin-positive group (P<0.001), although the groups were otherwise homogeneous. There was a statistically significant difference in the number of all types of refluxes between groups. Six or more pharyngeal refluxes were the cutoff for the presence of pepsin in the laryngeal mucosa and, thereby, for the diagnosis of relevant/pathological LPR. CONCLUSION:Six or more pharyngeal reflux episodes registered during the 24-h impedance/pH monitoring seem to be the cutoff for diagnosing pathological LPR. Therefore, it is possible to suggest establishing this value as the pathological impedance value indicating pathological LPR. These results must be interpreted with caution due to the small sample size.

Project description:The susceptibility of a dietary protein to proteolytic degradation by digestive enzymes, such as gastric pepsin, provides information on the likelihood of systemic exposure to a structurally intact and biologically active macromolecule, thus informing on the safety of proteins for human and animal consumption. Therefore, the purpose of standardized in vitro degradation studies that are performed during protein safety assessments is to distinguish whether proteins of interest are susceptible or resistant to pepsin degradation via a study design that enables study-to-study comparison. Attempting to assess pepsin degradation under a wide-range of possible physiological conditions poses a problem because of the lack of robust and consistent data collected under a large-range of sub-optimal conditions, which undermines the needs to harmonize in vitro degradation conditions. This report systematically compares the effects of pH, incubation time, and pepsin-to-substrate protein ratio on the relative degradation of five dietary proteins: three pepsin susceptible proteins [ribulose 1,5-bisphosphate carboxylase-oxygenase (Rubisco), horseradish peroxidase (HRP), hemoglobin (Hb)], and two pepsin resistant proteins [lipid transfer protein (LTP) and soybean trypsin inhibitor (STI)]. The results indicate that proteins susceptible to pepsin degradation are readily distinguishable from pepsin-resistant proteins when the reaction conditions are within the well-characterized optima for pepsin. The current standardized in vitro pepsin resistant assay with low pH and high pepsin-to-substrate ratio fits this purpose. Using non-optimal pH and/or pepsin-to-substrate protein ratios resulted in susceptible proteins no longer being reliably degraded by this stomach enzyme, which compromises the ability of this in vitro assay to distinguish between resistant and susceptible proteins and, therefore, no longer providing useful data to an overall weight-of-evidence approach to assessing safety of proteins.

Dataset Information

Effects of pepsin and pepstatin on reflux tonsil hypertrophy in vitro.

Publications

Effects of pepsin and pepstatin on reflux tonsil hypertrophy in vitro.

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