Se-methylselenocysteine inhibits inflammatory response in an LPS-stimulated chicken HD11 macrophage-like cell model through the NFKB2 pathway
Among the various sources of selenium supplementations, the Se-methylselenocysteine (SeMC) is a natural organic selenium compound that has been demonstrated to have multiple advantages in terms of metabolism efficiency and biosafety in animals. Nevertheless, the genome-wide impact of SeMC on gene tr...
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Frontiers Media S.A.
2025-01-01
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Online Access: | https://www.frontiersin.org/articles/10.3389/fvets.2024.1503436/full |
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author | Min Yao Binyu Wang Zitong Li Suqing Wu Bingyu Zhao Ning Sun Huiping Xiao Jianwu Wang Guoping Liu Tinghua Huang |
author_facet | Min Yao Binyu Wang Zitong Li Suqing Wu Bingyu Zhao Ning Sun Huiping Xiao Jianwu Wang Guoping Liu Tinghua Huang |
author_sort | Min Yao |
collection | DOAJ |
description | Among the various sources of selenium supplementations, the Se-methylselenocysteine (SeMC) is a natural organic selenium compound that has been demonstrated to have multiple advantages in terms of metabolism efficiency and biosafety in animals. Nevertheless, the genome-wide impact of SeMC on gene transcription remains to be elucidated. In this study, we employed an LPS-stimulated chicken HD11 macrophage-like cell model to identify the principal transcription factors involved in transcriptome regulation responsible for SeMC treatment. RNA-seq identified 3,263 transcripts that exhibited a statistically significant differential expression between the SeMC-treated group and the control group and 1,344 transcripts that exhibited a statistically significant differential expression between the LPS + SeMC- and LPS-treated groups (FDR < 0.05, FDR > 1.5). The bioinformatic analysis identified six transcription factors (NFKB2, RFX2, E2F5, ETV5, BACH1, and E2F7) as potential candidate genes for transcriptome regulation in SeMC-treated HD11 cells. Subsequent experimental verification demonstrated that SeMC suppressed the inflammatory response in an LPS-stimulated chicken HD11 cell model via the TXN2—NF-κB pathway. The administration SeMC was observed to reduce the production of ROS as well as the transcription and translation of inflammatory cytokines in both cell culture and in vivo animal studies. One candidate pathway by which SeMC exerts its effects is through the targeting of the transcription factor, NFKB2, by selenoprotein TXN2. This study identified key transcription factors and revealed one of the potential mechanisms through which SeMC exerts its anti-inflammatory effects from the perspective of transcriptional regulation. |
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institution | Kabale University |
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language | English |
publishDate | 2025-01-01 |
publisher | Frontiers Media S.A. |
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series | Frontiers in Veterinary Science |
spelling | doaj-art-6fdae2136e0542cbb8d3350431207a982025-01-08T06:11:59ZengFrontiers Media S.A.Frontiers in Veterinary Science2297-17692025-01-011110.3389/fvets.2024.15034361503436Se-methylselenocysteine inhibits inflammatory response in an LPS-stimulated chicken HD11 macrophage-like cell model through the NFKB2 pathwayMin Yao0Binyu Wang1Zitong Li2Suqing Wu3Bingyu Zhao4Ning Sun5Huiping Xiao6Jianwu Wang7Guoping Liu8Tinghua Huang9College of Animal Science and Technology, Yangtze University, Jingzhou, ChinaCollege of Animal Science and Technology, Yangtze University, Jingzhou, ChinaCollege of Animal Science and Technology, Yangtze University, Jingzhou, ChinaCollege of Animal Science and Technology, Yangtze University, Jingzhou, ChinaCollege of Animal Science and Technology, Yangtze University, Jingzhou, ChinaCollege of Animal Science and Technology, Yangtze University, Jingzhou, ChinaCollege of Animal Science and Technology, Yangtze University, Jingzhou, ChinaCollege of Agriculture, Yangtze University, Jingzhou, ChinaCollege of Animal Science and Technology, Yangtze University, Jingzhou, ChinaCollege of Animal Science and Technology, Yangtze University, Jingzhou, ChinaAmong the various sources of selenium supplementations, the Se-methylselenocysteine (SeMC) is a natural organic selenium compound that has been demonstrated to have multiple advantages in terms of metabolism efficiency and biosafety in animals. Nevertheless, the genome-wide impact of SeMC on gene transcription remains to be elucidated. In this study, we employed an LPS-stimulated chicken HD11 macrophage-like cell model to identify the principal transcription factors involved in transcriptome regulation responsible for SeMC treatment. RNA-seq identified 3,263 transcripts that exhibited a statistically significant differential expression between the SeMC-treated group and the control group and 1,344 transcripts that exhibited a statistically significant differential expression between the LPS + SeMC- and LPS-treated groups (FDR < 0.05, FDR > 1.5). The bioinformatic analysis identified six transcription factors (NFKB2, RFX2, E2F5, ETV5, BACH1, and E2F7) as potential candidate genes for transcriptome regulation in SeMC-treated HD11 cells. Subsequent experimental verification demonstrated that SeMC suppressed the inflammatory response in an LPS-stimulated chicken HD11 cell model via the TXN2—NF-κB pathway. The administration SeMC was observed to reduce the production of ROS as well as the transcription and translation of inflammatory cytokines in both cell culture and in vivo animal studies. One candidate pathway by which SeMC exerts its effects is through the targeting of the transcription factor, NFKB2, by selenoprotein TXN2. This study identified key transcription factors and revealed one of the potential mechanisms through which SeMC exerts its anti-inflammatory effects from the perspective of transcriptional regulation.https://www.frontiersin.org/articles/10.3389/fvets.2024.1503436/fullse-methyselenocysteineinflammatory responseHD11NFKB2chicken |
spellingShingle | Min Yao Binyu Wang Zitong Li Suqing Wu Bingyu Zhao Ning Sun Huiping Xiao Jianwu Wang Guoping Liu Tinghua Huang Se-methylselenocysteine inhibits inflammatory response in an LPS-stimulated chicken HD11 macrophage-like cell model through the NFKB2 pathway Frontiers in Veterinary Science se-methyselenocysteine inflammatory response HD11 NFKB2 chicken |
title | Se-methylselenocysteine inhibits inflammatory response in an LPS-stimulated chicken HD11 macrophage-like cell model through the NFKB2 pathway |
title_full | Se-methylselenocysteine inhibits inflammatory response in an LPS-stimulated chicken HD11 macrophage-like cell model through the NFKB2 pathway |
title_fullStr | Se-methylselenocysteine inhibits inflammatory response in an LPS-stimulated chicken HD11 macrophage-like cell model through the NFKB2 pathway |
title_full_unstemmed | Se-methylselenocysteine inhibits inflammatory response in an LPS-stimulated chicken HD11 macrophage-like cell model through the NFKB2 pathway |
title_short | Se-methylselenocysteine inhibits inflammatory response in an LPS-stimulated chicken HD11 macrophage-like cell model through the NFKB2 pathway |
title_sort | se methylselenocysteine inhibits inflammatory response in an lps stimulated chicken hd11 macrophage like cell model through the nfkb2 pathway |
topic | se-methyselenocysteine inflammatory response HD11 NFKB2 chicken |
url | https://www.frontiersin.org/articles/10.3389/fvets.2024.1503436/full |
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