Vitamin D(3) deficiency induced intestinal inflammatory response of turbot through nuclear factor-κB/inflammasome pathway, accompanied by the mutually exclusive apoptosis and autophagy
Vitamin D(3) (VD(3)) participated widely in the nuclear factor-κB (NF-κB)-mediated inflammation, apoptosis, and autophagy through the vitamin D receptor (VDR). However, the molecular mechanisms remain not understood in teleost. The present study investigated the functions of VD(3)/VDR on intestinal...
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ftpubmed:oai:pubmedcentral.nih.gov:9493454 2023-05-15T18:41:09+02:00 Vitamin D(3) deficiency induced intestinal inflammatory response of turbot through nuclear factor-κB/inflammasome pathway, accompanied by the mutually exclusive apoptosis and autophagy Chen, Zhichu Huang, Dong Yongyut, Prakaiwan Li, Guangbin Esteban, María Ángeles Jintasataporn, Orapint Deng, Junming Zhang, Wenbing Ai, Qinghui Mai, Kangsen Zhang, Yanjiao 2022-09-08 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9493454/ https://doi.org/10.3389/fimmu.2022.986593 en eng Frontiers Media S.A. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9493454/ http://dx.doi.org/10.3389/fimmu.2022.986593 Copyright © 2022 Chen, Huang, Yongyut, Li, Esteban, Jintasataporn, Deng, Zhang, Ai, Mai and Zhang https://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. CC-BY Front Immunol Immunology Text 2022 ftpubmed https://doi.org/10.3389/fimmu.2022.986593 2022-09-25T01:08:46Z Vitamin D(3) (VD(3)) participated widely in the nuclear factor-κB (NF-κB)-mediated inflammation, apoptosis, and autophagy through the vitamin D receptor (VDR). However, the molecular mechanisms remain not understood in teleost. The present study investigated the functions of VD(3)/VDR on intestinal inflammation, autophagy, and apoptosis of turbot in vivo and in vitro. Triple replicates of 30 fish were fed with each of three diets with graded levels of 32.0 (D(0)), 1012.6 (D(1)), and 3978.2 (D(2)) IU/kg VD(3). Obvious intestinal enteritis was observed in the D(0) group and followed with dysfunction of intestinal mucosal barriers. The intestinal inflammatory response induced by VD(3) deficiency was regulated by the NF-κB/inflammasome signalling. The promotion of intestinal apoptosis and suppression of intestinal autophagy were also observed in the D(0) group. Similarly, VD(3) deficiency in vitro induced more intense inflammation regulated by NF-κB/inflammasome signalling. The mutually exclusive apoptosis and autophagy were also observed in the group without 1,25(OH)(2)D(3) in vitro, accompanied by similar changes in apoptosis and autophagy increased apoptosis. The gene expression of VDRs was significantly increased with the increasing VD(3) supplementation both in vivo and in vitro. Moreover, VDR knockdown in turbot resulted in intestinal inflammation, and this process relied on the activation of inflammasome mediated by NF-κB signalling. Simultaneously, intestinal apoptosis was promoted, whereas intestinal autophagy was inhibited. In conclusion, VD(3) deficiency could induce intestinal inflammation via activation of the NF-κB/inflammasome pathway, intestinal apoptosis, and autophagy formed a mutually exclusive relation in teleost. And VDR is the critical molecule in those processes. Text Turbot PubMed Central (PMC) Frontiers in Immunology 13 |
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Immunology |
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Immunology Chen, Zhichu Huang, Dong Yongyut, Prakaiwan Li, Guangbin Esteban, María Ángeles Jintasataporn, Orapint Deng, Junming Zhang, Wenbing Ai, Qinghui Mai, Kangsen Zhang, Yanjiao Vitamin D(3) deficiency induced intestinal inflammatory response of turbot through nuclear factor-κB/inflammasome pathway, accompanied by the mutually exclusive apoptosis and autophagy |
topic_facet |
Immunology |
description |
Vitamin D(3) (VD(3)) participated widely in the nuclear factor-κB (NF-κB)-mediated inflammation, apoptosis, and autophagy through the vitamin D receptor (VDR). However, the molecular mechanisms remain not understood in teleost. The present study investigated the functions of VD(3)/VDR on intestinal inflammation, autophagy, and apoptosis of turbot in vivo and in vitro. Triple replicates of 30 fish were fed with each of three diets with graded levels of 32.0 (D(0)), 1012.6 (D(1)), and 3978.2 (D(2)) IU/kg VD(3). Obvious intestinal enteritis was observed in the D(0) group and followed with dysfunction of intestinal mucosal barriers. The intestinal inflammatory response induced by VD(3) deficiency was regulated by the NF-κB/inflammasome signalling. The promotion of intestinal apoptosis and suppression of intestinal autophagy were also observed in the D(0) group. Similarly, VD(3) deficiency in vitro induced more intense inflammation regulated by NF-κB/inflammasome signalling. The mutually exclusive apoptosis and autophagy were also observed in the group without 1,25(OH)(2)D(3) in vitro, accompanied by similar changes in apoptosis and autophagy increased apoptosis. The gene expression of VDRs was significantly increased with the increasing VD(3) supplementation both in vivo and in vitro. Moreover, VDR knockdown in turbot resulted in intestinal inflammation, and this process relied on the activation of inflammasome mediated by NF-κB signalling. Simultaneously, intestinal apoptosis was promoted, whereas intestinal autophagy was inhibited. In conclusion, VD(3) deficiency could induce intestinal inflammation via activation of the NF-κB/inflammasome pathway, intestinal apoptosis, and autophagy formed a mutually exclusive relation in teleost. And VDR is the critical molecule in those processes. |
format |
Text |
author |
Chen, Zhichu Huang, Dong Yongyut, Prakaiwan Li, Guangbin Esteban, María Ángeles Jintasataporn, Orapint Deng, Junming Zhang, Wenbing Ai, Qinghui Mai, Kangsen Zhang, Yanjiao |
author_facet |
Chen, Zhichu Huang, Dong Yongyut, Prakaiwan Li, Guangbin Esteban, María Ángeles Jintasataporn, Orapint Deng, Junming Zhang, Wenbing Ai, Qinghui Mai, Kangsen Zhang, Yanjiao |
author_sort |
Chen, Zhichu |
title |
Vitamin D(3) deficiency induced intestinal inflammatory response of turbot through nuclear factor-κB/inflammasome pathway, accompanied by the mutually exclusive apoptosis and autophagy |
title_short |
Vitamin D(3) deficiency induced intestinal inflammatory response of turbot through nuclear factor-κB/inflammasome pathway, accompanied by the mutually exclusive apoptosis and autophagy |
title_full |
Vitamin D(3) deficiency induced intestinal inflammatory response of turbot through nuclear factor-κB/inflammasome pathway, accompanied by the mutually exclusive apoptosis and autophagy |
title_fullStr |
Vitamin D(3) deficiency induced intestinal inflammatory response of turbot through nuclear factor-κB/inflammasome pathway, accompanied by the mutually exclusive apoptosis and autophagy |
title_full_unstemmed |
Vitamin D(3) deficiency induced intestinal inflammatory response of turbot through nuclear factor-κB/inflammasome pathway, accompanied by the mutually exclusive apoptosis and autophagy |
title_sort |
vitamin d(3) deficiency induced intestinal inflammatory response of turbot through nuclear factor-κb/inflammasome pathway, accompanied by the mutually exclusive apoptosis and autophagy |
publisher |
Frontiers Media S.A. |
publishDate |
2022 |
url |
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9493454/ https://doi.org/10.3389/fimmu.2022.986593 |
genre |
Turbot |
genre_facet |
Turbot |
op_source |
Front Immunol |
op_relation |
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9493454/ http://dx.doi.org/10.3389/fimmu.2022.986593 |
op_rights |
Copyright © 2022 Chen, Huang, Yongyut, Li, Esteban, Jintasataporn, Deng, Zhang, Ai, Mai and Zhang https://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. |
op_rightsnorm |
CC-BY |
op_doi |
https://doi.org/10.3389/fimmu.2022.986593 |
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Frontiers in Immunology |
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13 |
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1766230642903744512 |