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NLRP3 played a role in Trichinella spiralis-triggered Th2 and regulatory T cells response

Trichinella spiralis maintains chronic infections within its host. Muscle larvae excretory-secretory products (MLES) typically induce parasite-specific immune responses such as the Th2 response and regulatory T cells (Tregs) by modulating dendritic cell (DC) phenotype via the recognition of pattern...

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Autores principales: Jin, Xuemin, Bai, Xue, Yang, Yong, Ding, Jing, Shi, Haining, Fu, Baoquan, Boireau, Pascal, Liu, Mingyuan, Liu, Xiaolei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7457311/
https://www.ncbi.nlm.nih.gov/pubmed/32854770
http://dx.doi.org/10.1186/s13567-020-00829-2
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author Jin, Xuemin
Bai, Xue
Yang, Yong
Ding, Jing
Shi, Haining
Fu, Baoquan
Boireau, Pascal
Liu, Mingyuan
Liu, Xiaolei
author_facet Jin, Xuemin
Bai, Xue
Yang, Yong
Ding, Jing
Shi, Haining
Fu, Baoquan
Boireau, Pascal
Liu, Mingyuan
Liu, Xiaolei
author_sort Jin, Xuemin
collection PubMed
description Trichinella spiralis maintains chronic infections within its host. Muscle larvae excretory-secretory products (MLES) typically induce parasite-specific immune responses such as the Th2 response and regulatory T cells (Tregs) by modulating dendritic cell (DC) phenotype via the recognition of pattern recognition receptors (PRRs), such as Nod-like receptors (NLRs). We aimed to investigate the role of NLRP3 in T. spiralis-triggered immune response. We found that larvae burden was increased in NLRP3(−/−) mice compared to wild type (WT) mice. Administration of MLES induced higher levels of IL-4, IL-10, TGF-β and population of Tregs in WT mice than in NLRP3(−/−) mice. In vitro, we showed that increased expression of CD40 on the surface of MLES-treated DCs was inhibited after NLRP3 knockout. Increased production of IL-1β, IL-18, IL-10 and TGF-β, but not IL-12p70, was significantly diminished in the absence of NLRP3. Furthermore, our results demonstrated that MLES-treated DCs induced higher levels of IL-4, IL-10 and TGF-β and populations of Tregs in vitro. These inductions were abolished by NLRP3 deficiency in DCs, suggesting that NLRP3 in MLES-treated DCs plays a role in promoting the Th2 and Treg response. Taken together, we identified for the first time the involvement of NLRP3 in host defences against T. spiralis.
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spelling pubmed-74573112020-08-31 NLRP3 played a role in Trichinella spiralis-triggered Th2 and regulatory T cells response Jin, Xuemin Bai, Xue Yang, Yong Ding, Jing Shi, Haining Fu, Baoquan Boireau, Pascal Liu, Mingyuan Liu, Xiaolei Vet Res Research Article Trichinella spiralis maintains chronic infections within its host. Muscle larvae excretory-secretory products (MLES) typically induce parasite-specific immune responses such as the Th2 response and regulatory T cells (Tregs) by modulating dendritic cell (DC) phenotype via the recognition of pattern recognition receptors (PRRs), such as Nod-like receptors (NLRs). We aimed to investigate the role of NLRP3 in T. spiralis-triggered immune response. We found that larvae burden was increased in NLRP3(−/−) mice compared to wild type (WT) mice. Administration of MLES induced higher levels of IL-4, IL-10, TGF-β and population of Tregs in WT mice than in NLRP3(−/−) mice. In vitro, we showed that increased expression of CD40 on the surface of MLES-treated DCs was inhibited after NLRP3 knockout. Increased production of IL-1β, IL-18, IL-10 and TGF-β, but not IL-12p70, was significantly diminished in the absence of NLRP3. Furthermore, our results demonstrated that MLES-treated DCs induced higher levels of IL-4, IL-10 and TGF-β and populations of Tregs in vitro. These inductions were abolished by NLRP3 deficiency in DCs, suggesting that NLRP3 in MLES-treated DCs plays a role in promoting the Th2 and Treg response. Taken together, we identified for the first time the involvement of NLRP3 in host defences against T. spiralis. BioMed Central 2020-08-27 2020 /pmc/articles/PMC7457311/ /pubmed/32854770 http://dx.doi.org/10.1186/s13567-020-00829-2 Text en © The Author(s) 2020 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research Article
Jin, Xuemin
Bai, Xue
Yang, Yong
Ding, Jing
Shi, Haining
Fu, Baoquan
Boireau, Pascal
Liu, Mingyuan
Liu, Xiaolei
NLRP3 played a role in Trichinella spiralis-triggered Th2 and regulatory T cells response
title NLRP3 played a role in Trichinella spiralis-triggered Th2 and regulatory T cells response
title_full NLRP3 played a role in Trichinella spiralis-triggered Th2 and regulatory T cells response
title_fullStr NLRP3 played a role in Trichinella spiralis-triggered Th2 and regulatory T cells response
title_full_unstemmed NLRP3 played a role in Trichinella spiralis-triggered Th2 and regulatory T cells response
title_short NLRP3 played a role in Trichinella spiralis-triggered Th2 and regulatory T cells response
title_sort nlrp3 played a role in trichinella spiralis-triggered th2 and regulatory t cells response
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7457311/
https://www.ncbi.nlm.nih.gov/pubmed/32854770
http://dx.doi.org/10.1186/s13567-020-00829-2
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