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Effects of pepsin and pepstatin on reflux tonsil hypertrophy in vitro

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...

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Autores principales: Kim, Jin Hyun, Jang, Si Jung, Yun, Jeong Won, Jung, Myeong Hee, Woo, Seung Hoon
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6224077/
https://www.ncbi.nlm.nih.gov/pubmed/30408092
http://dx.doi.org/10.1371/journal.pone.0207090
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author Kim, Jin Hyun
Jang, Si Jung
Yun, Jeong Won
Jung, Myeong Hee
Woo, Seung Hoon
author_facet Kim, Jin Hyun
Jang, Si Jung
Yun, Jeong Won
Jung, Myeong Hee
Woo, Seung Hoon
author_sort Kim, Jin Hyun
collection PubMed
description 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-γ) 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.
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spelling pubmed-62240772018-11-19 Effects of pepsin and pepstatin on reflux tonsil hypertrophy in vitro Kim, Jin Hyun Jang, Si Jung Yun, Jeong Won Jung, Myeong Hee Woo, Seung Hoon PLoS One Research Article 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-γ) 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. Public Library of Science 2018-11-08 /pmc/articles/PMC6224077/ /pubmed/30408092 http://dx.doi.org/10.1371/journal.pone.0207090 Text en © 2018 Kim et al http://creativecommons.org/licenses/by/4.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/) , which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Article
Kim, Jin Hyun
Jang, Si Jung
Yun, Jeong Won
Jung, Myeong Hee
Woo, Seung Hoon
Effects of pepsin and pepstatin on reflux tonsil hypertrophy in vitro
title Effects of pepsin and pepstatin on reflux tonsil hypertrophy in vitro
title_full Effects of pepsin and pepstatin on reflux tonsil hypertrophy in vitro
title_fullStr Effects of pepsin and pepstatin on reflux tonsil hypertrophy in vitro
title_full_unstemmed Effects of pepsin and pepstatin on reflux tonsil hypertrophy in vitro
title_short Effects of pepsin and pepstatin on reflux tonsil hypertrophy in vitro
title_sort effects of pepsin and pepstatin on reflux tonsil hypertrophy in vitro
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6224077/
https://www.ncbi.nlm.nih.gov/pubmed/30408092
http://dx.doi.org/10.1371/journal.pone.0207090
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