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Regulation of Endotoxin Tolerance and Compensatory Anti-inflammatory Response Syndrome by Non-coding RNAs
The onset and the termination of innate immune response must be tightly regulated to maintain homeostasis and prevent excessive inflammation, which can be detrimental to the organism, particularly in the context of sepsis. Endotoxin tolerance and compensatory anti-inflammatory response syndrome (CAR...
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2018
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6255943/ https://www.ncbi.nlm.nih.gov/pubmed/30515175 http://dx.doi.org/10.3389/fimmu.2018.02705 |
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author | Vergadi, Eleni Vaporidi, Katerina Tsatsanis, Christos |
author_facet | Vergadi, Eleni Vaporidi, Katerina Tsatsanis, Christos |
author_sort | Vergadi, Eleni |
collection | PubMed |
description | The onset and the termination of innate immune response must be tightly regulated to maintain homeostasis and prevent excessive inflammation, which can be detrimental to the organism, particularly in the context of sepsis. Endotoxin tolerance and compensatory anti-inflammatory response syndrome (CARS) describe a state of hypo-responsiveness characterized by reduced capacity of myeloid cells to respond to inflammatory stimuli, particularly those initiated by bacterial lipopolysaccharide (LPS). To achieve endotoxin tolerance, extensive reprogramming otherwise termed as “innate immune training”, is required that leads to both modifications of the intracellular components of TLR signaling and also to alterations in extracellular soluble mediators. Non-coding RNAs (ncRNAs) have been recognized as critical regulators of TLR signaling. Specifically, several microRNAs (miR-146, miR-125b, miR-98, miR-579, miR-132, let-7e and others) are induced upon TLR activation and reciprocally promote endotoxin tolerance and/or cross tolerance. Many other miRNAs have been also shown to negatively regulate TLR signaling. The long non-coding (lnc)RNAs (Mirt2, THRIL, MALAT1, lincRNA-21 and others) are also altered upon TLR activation and negatively regulate TLR signaling. Furthermore, the promotion or termination of myeloid cell tolerance is not only regulated by intracellular mediators but is also affected by other TLR-independent soluble signals that often achieve their effect via modulation of intracellular ncRNAs. In this article, we review recent evidence on the role of different ncRNAs in the context of innate immune cell tolerance and trained immunity, and evaluate their impact on immune system homeostasis. |
format | Online Article Text |
id | pubmed-6255943 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-62559432018-12-04 Regulation of Endotoxin Tolerance and Compensatory Anti-inflammatory Response Syndrome by Non-coding RNAs Vergadi, Eleni Vaporidi, Katerina Tsatsanis, Christos Front Immunol Immunology The onset and the termination of innate immune response must be tightly regulated to maintain homeostasis and prevent excessive inflammation, which can be detrimental to the organism, particularly in the context of sepsis. Endotoxin tolerance and compensatory anti-inflammatory response syndrome (CARS) describe a state of hypo-responsiveness characterized by reduced capacity of myeloid cells to respond to inflammatory stimuli, particularly those initiated by bacterial lipopolysaccharide (LPS). To achieve endotoxin tolerance, extensive reprogramming otherwise termed as “innate immune training”, is required that leads to both modifications of the intracellular components of TLR signaling and also to alterations in extracellular soluble mediators. Non-coding RNAs (ncRNAs) have been recognized as critical regulators of TLR signaling. Specifically, several microRNAs (miR-146, miR-125b, miR-98, miR-579, miR-132, let-7e and others) are induced upon TLR activation and reciprocally promote endotoxin tolerance and/or cross tolerance. Many other miRNAs have been also shown to negatively regulate TLR signaling. The long non-coding (lnc)RNAs (Mirt2, THRIL, MALAT1, lincRNA-21 and others) are also altered upon TLR activation and negatively regulate TLR signaling. Furthermore, the promotion or termination of myeloid cell tolerance is not only regulated by intracellular mediators but is also affected by other TLR-independent soluble signals that often achieve their effect via modulation of intracellular ncRNAs. In this article, we review recent evidence on the role of different ncRNAs in the context of innate immune cell tolerance and trained immunity, and evaluate their impact on immune system homeostasis. Frontiers Media S.A. 2018-11-20 /pmc/articles/PMC6255943/ /pubmed/30515175 http://dx.doi.org/10.3389/fimmu.2018.02705 Text en Copyright © 2018 Vergadi, Vaporidi and Tsatsanis. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Immunology Vergadi, Eleni Vaporidi, Katerina Tsatsanis, Christos Regulation of Endotoxin Tolerance and Compensatory Anti-inflammatory Response Syndrome by Non-coding RNAs |
title | Regulation of Endotoxin Tolerance and Compensatory Anti-inflammatory Response Syndrome by Non-coding RNAs |
title_full | Regulation of Endotoxin Tolerance and Compensatory Anti-inflammatory Response Syndrome by Non-coding RNAs |
title_fullStr | Regulation of Endotoxin Tolerance and Compensatory Anti-inflammatory Response Syndrome by Non-coding RNAs |
title_full_unstemmed | Regulation of Endotoxin Tolerance and Compensatory Anti-inflammatory Response Syndrome by Non-coding RNAs |
title_short | Regulation of Endotoxin Tolerance and Compensatory Anti-inflammatory Response Syndrome by Non-coding RNAs |
title_sort | regulation of endotoxin tolerance and compensatory anti-inflammatory response syndrome by non-coding rnas |
topic | Immunology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6255943/ https://www.ncbi.nlm.nih.gov/pubmed/30515175 http://dx.doi.org/10.3389/fimmu.2018.02705 |
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