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Asthma and obesity: endotoxin another insult to add to injury?
Low-grade inflammation is often an underlying cause of several chronic diseases such as asthma, obesity, cardiovascular disease, and type 2 diabetes mellitus (T2DM). Defining the mediators of such chronic low-grade inflammation often appears dependent on which disease is being investigated. However,...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Portland Press Ltd.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8689194/ https://www.ncbi.nlm.nih.gov/pubmed/34918742 http://dx.doi.org/10.1042/CS20210790 |
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author | Lad, Nikita Murphy, Alice M. Parenti, Cristina Nelson, Carl P. Williams, Neil C. Sharpe, Graham R. McTernan, Philip G. |
author_facet | Lad, Nikita Murphy, Alice M. Parenti, Cristina Nelson, Carl P. Williams, Neil C. Sharpe, Graham R. McTernan, Philip G. |
author_sort | Lad, Nikita |
collection | PubMed |
description | Low-grade inflammation is often an underlying cause of several chronic diseases such as asthma, obesity, cardiovascular disease, and type 2 diabetes mellitus (T2DM). Defining the mediators of such chronic low-grade inflammation often appears dependent on which disease is being investigated. However, downstream systemic inflammatory cytokine responses in these diseases often overlap, noting there is no doubt more than one factor at play to heighten the inflammatory response. Furthermore, it is increasingly believed that diet and an altered gut microbiota may play an important role in the pathology of such diverse diseases. More specifically, the inflammatory mediator endotoxin, which is a complex lipopolysaccharide (LPS) derived from the outer membrane cell wall of Gram-negative bacteria and is abundant within the gut microbiota, and may play a direct role alongside inhaled allergens in eliciting an inflammatory response in asthma. Endotoxin has immunogenic effects and is sufficiently microscopic to traverse the gut mucosa and enter the systemic circulation to act as a mediator of chronic low-grade inflammation in disease. Whilst the role of endotoxin has been considered in conditions of obesity, cardiovascular disease and T2DM, endotoxin as an inflammatory trigger in asthma is less well understood. This review has sought to examine the current evidence for the role of endotoxin in asthma, and whether the gut microbiota could be a dietary target to improve disease management. This may expand our understanding of endotoxin as a mediator of further low-grade inflammatory diseases, and how endotoxin may represent yet another insult to add to injury. |
format | Online Article Text |
id | pubmed-8689194 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | Portland Press Ltd. |
record_format | MEDLINE/PubMed |
spelling | pubmed-86891942022-01-04 Asthma and obesity: endotoxin another insult to add to injury? Lad, Nikita Murphy, Alice M. Parenti, Cristina Nelson, Carl P. Williams, Neil C. Sharpe, Graham R. McTernan, Philip G. Clin Sci (Lond) Diabetes & Metabolic Disorders Low-grade inflammation is often an underlying cause of several chronic diseases such as asthma, obesity, cardiovascular disease, and type 2 diabetes mellitus (T2DM). Defining the mediators of such chronic low-grade inflammation often appears dependent on which disease is being investigated. However, downstream systemic inflammatory cytokine responses in these diseases often overlap, noting there is no doubt more than one factor at play to heighten the inflammatory response. Furthermore, it is increasingly believed that diet and an altered gut microbiota may play an important role in the pathology of such diverse diseases. More specifically, the inflammatory mediator endotoxin, which is a complex lipopolysaccharide (LPS) derived from the outer membrane cell wall of Gram-negative bacteria and is abundant within the gut microbiota, and may play a direct role alongside inhaled allergens in eliciting an inflammatory response in asthma. Endotoxin has immunogenic effects and is sufficiently microscopic to traverse the gut mucosa and enter the systemic circulation to act as a mediator of chronic low-grade inflammation in disease. Whilst the role of endotoxin has been considered in conditions of obesity, cardiovascular disease and T2DM, endotoxin as an inflammatory trigger in asthma is less well understood. This review has sought to examine the current evidence for the role of endotoxin in asthma, and whether the gut microbiota could be a dietary target to improve disease management. This may expand our understanding of endotoxin as a mediator of further low-grade inflammatory diseases, and how endotoxin may represent yet another insult to add to injury. Portland Press Ltd. 2021-12 2021-12-17 /pmc/articles/PMC8689194/ /pubmed/34918742 http://dx.doi.org/10.1042/CS20210790 Text en © 2021 The Author(s). https://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (https://creativecommons.org/licenses/by/4.0/) . |
spellingShingle | Diabetes & Metabolic Disorders Lad, Nikita Murphy, Alice M. Parenti, Cristina Nelson, Carl P. Williams, Neil C. Sharpe, Graham R. McTernan, Philip G. Asthma and obesity: endotoxin another insult to add to injury? |
title | Asthma and obesity: endotoxin another insult to add to injury? |
title_full | Asthma and obesity: endotoxin another insult to add to injury? |
title_fullStr | Asthma and obesity: endotoxin another insult to add to injury? |
title_full_unstemmed | Asthma and obesity: endotoxin another insult to add to injury? |
title_short | Asthma and obesity: endotoxin another insult to add to injury? |
title_sort | asthma and obesity: endotoxin another insult to add to injury? |
topic | Diabetes & Metabolic Disorders |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8689194/ https://www.ncbi.nlm.nih.gov/pubmed/34918742 http://dx.doi.org/10.1042/CS20210790 |
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