Asthma and obesity: endotoxin another insult to add to injury?

Lad, N., Murphy, A.M. ORCID: 0000-0001-5554-1558, Parenti, C. ORCID: 0000-0003-3439-5816, Nelson, C.P. ORCID: 0000-0003-1034-140X, Williams, N.C. ORCID: 0000-0002-2607-4572, Sharpe, G.R. ORCID: 0000-0002-4575-2332 and McTernan, P.G. ORCID: 0000-0001-9023-0261, 2021. Asthma and obesity: endotoxin another insult to add to injury? Clinical Science, 135 (24), pp. 2729-2748. ISSN 0143-5221

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Abstract

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.

Item Type: Journal article
Publication Title: Clinical Science
Creators: Lad, N., Murphy, A.M., Parenti, C., Nelson, C.P., Williams, N.C., Sharpe, G.R. and McTernan, P.G.
Publisher: Portland Press Ltd.
Date: 22 December 2021
Volume: 135
Number: 24
ISSN: 0143-5221
Identifiers:
NumberType
10.1042/cs20210790DOI
1509771Other
Rights: © 2021 The Author(s). 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).
Divisions: Schools > School of Science and Technology
Record created by: Jeremy Silvester
Date Added: 20 Jan 2022 16:13
Last Modified: 20 Jan 2022 16:13
URI: http://irep.ntu.ac.uk/id/eprint/45378

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