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HMGB1 in the Pathogenesis of Nasal Inflammatory Diseases and its Inhibition as New Therapeutic Approach: A Review from the Literature

Introduction  This study is a systematic review on recent developments about the importance of HMGB1 protein in the pathogenesis of rhino-sinusal inflammatory diseases. We also report data on the use of 18-β-glycyrrhetic acid (GA), which has been shown able to inhibit the pro-inflammatory activities...

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Autores principales: Bellussi, Luisa Maria, Cocca, Serena, Passali, Giulio Cesare, Passali, Desideri
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Thieme Revinter Publicações Ltda 2017
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5629088/
https://www.ncbi.nlm.nih.gov/pubmed/29018504
http://dx.doi.org/10.1055/s-0036-1597665
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author Bellussi, Luisa Maria
Cocca, Serena
Passali, Giulio Cesare
Passali, Desideri
author_facet Bellussi, Luisa Maria
Cocca, Serena
Passali, Giulio Cesare
Passali, Desideri
author_sort Bellussi, Luisa Maria
collection PubMed
description Introduction  This study is a systematic review on recent developments about the importance of HMGB1 protein in the pathogenesis of rhino-sinusal inflammatory diseases. We also report data on the use of 18-β-glycyrrhetic acid (GA), which has been shown able to inhibit the pro-inflammatory activities of HMGB1, in young patients affected by allergic rhinitis and complaining of nasal obstruction as main symptom. Objectives  The objective of this study was to review the literature to demonstrate the importance of HMGB1 in the pathogenesis of nasal inflammatory disorders and understand whether the inhibition of this protein may be an efficacious and innovative therapeutic strategy for patients with rhino-sinusal inflammation. Data Synthesis  Authors searched for pertinent articles indexed in PubMed, Scopus, and other health journals between 2004 and 2015. In total, the authors gathered 258 articles: 219 articles through Pubmed and 39 articles from other search engines. The search terms used were as follows: HMGB1 AND “respiratory epithelium,” “airway inflammation,” “rhinitis,” “allergic rhinitis,” “rhinosinusitis,” “nasal polyposis,” “glycyrrhetic acid,” “children.” Conclusions  Patients with severe symptoms have the highest serum levels and the highest extracellular expression of HMGB1. GA inhibits HMGB1 chemotactic and mitogenic function by a scavenger mechanism on extracellular HMGB1 accumulation stimulated by lipopolysaccharides in vitro. Treatment of allergic rhinitis with GA is not associated with local or systemic side effects in children and adults.
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spelling pubmed-56290882017-10-10 HMGB1 in the Pathogenesis of Nasal Inflammatory Diseases and its Inhibition as New Therapeutic Approach: A Review from the Literature Bellussi, Luisa Maria Cocca, Serena Passali, Giulio Cesare Passali, Desideri Int Arch Otorhinolaryngol Introduction  This study is a systematic review on recent developments about the importance of HMGB1 protein in the pathogenesis of rhino-sinusal inflammatory diseases. We also report data on the use of 18-β-glycyrrhetic acid (GA), which has been shown able to inhibit the pro-inflammatory activities of HMGB1, in young patients affected by allergic rhinitis and complaining of nasal obstruction as main symptom. Objectives  The objective of this study was to review the literature to demonstrate the importance of HMGB1 in the pathogenesis of nasal inflammatory disorders and understand whether the inhibition of this protein may be an efficacious and innovative therapeutic strategy for patients with rhino-sinusal inflammation. Data Synthesis  Authors searched for pertinent articles indexed in PubMed, Scopus, and other health journals between 2004 and 2015. In total, the authors gathered 258 articles: 219 articles through Pubmed and 39 articles from other search engines. The search terms used were as follows: HMGB1 AND “respiratory epithelium,” “airway inflammation,” “rhinitis,” “allergic rhinitis,” “rhinosinusitis,” “nasal polyposis,” “glycyrrhetic acid,” “children.” Conclusions  Patients with severe symptoms have the highest serum levels and the highest extracellular expression of HMGB1. GA inhibits HMGB1 chemotactic and mitogenic function by a scavenger mechanism on extracellular HMGB1 accumulation stimulated by lipopolysaccharides in vitro. Treatment of allergic rhinitis with GA is not associated with local or systemic side effects in children and adults. Thieme Revinter Publicações Ltda 2017-10 2017-01-04 /pmc/articles/PMC5629088/ /pubmed/29018504 http://dx.doi.org/10.1055/s-0036-1597665 Text en https://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivatives License, which permits unrestricted reproduction and distribution, for non-commercial purposes only; and use and reproduction, but not distribution, of adapted material for non-commercial purposes only, provided the original work is properly cited.
spellingShingle Bellussi, Luisa Maria
Cocca, Serena
Passali, Giulio Cesare
Passali, Desideri
HMGB1 in the Pathogenesis of Nasal Inflammatory Diseases and its Inhibition as New Therapeutic Approach: A Review from the Literature
title HMGB1 in the Pathogenesis of Nasal Inflammatory Diseases and its Inhibition as New Therapeutic Approach: A Review from the Literature
title_full HMGB1 in the Pathogenesis of Nasal Inflammatory Diseases and its Inhibition as New Therapeutic Approach: A Review from the Literature
title_fullStr HMGB1 in the Pathogenesis of Nasal Inflammatory Diseases and its Inhibition as New Therapeutic Approach: A Review from the Literature
title_full_unstemmed HMGB1 in the Pathogenesis of Nasal Inflammatory Diseases and its Inhibition as New Therapeutic Approach: A Review from the Literature
title_short HMGB1 in the Pathogenesis of Nasal Inflammatory Diseases and its Inhibition as New Therapeutic Approach: A Review from the Literature
title_sort hmgb1 in the pathogenesis of nasal inflammatory diseases and its inhibition as new therapeutic approach: a review from the literature
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5629088/
https://www.ncbi.nlm.nih.gov/pubmed/29018504
http://dx.doi.org/10.1055/s-0036-1597665
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