Gut microbiota contribution to selenium deficiency-induced gut-liver inflammation
© 2023 International Union of Biochemistry and Molecular Biology..
There is limited knowledge about the factors that drive gut-liver axis changes after selenium (Se) deficiency-induced gut or liver injuries. Thus, we tested Se deficiency in mice to determine its effects on intestinal bacterial balance and whether it induced liver injury. Serum Se concentration, lipopolysaccharide (LPS) level, and liver injury biomarkers were tested using a biochemical method, while pathological changes in the liver and jejunum were observed via hematoxylin and eosin stain, and a fluorescence spectrophotometer was used to evaluate intestinal permeability. Tight junction (TJ)-related and toll-like receptor (TLR) signaling-related pathway genes and proteins were tested using quantitative polymerase chain reaction, western blotting, immunohistochemistry, and 16S ribosomal ribonucleic acid gene-targeted sequencing of jejunum microorganisms. Se deficiency significantly decreased glutathione peroxidase activity and disrupted the intestinal flora, with the most significant effect being a decrease in Lactobacillus reuteri. The expression of TJ-related genes and proteins decreased significantly with increased treatment time, whereas supplementation with Se, fecal microbiota transplantation, or L. reuteri reversed these decreases. Signs of liver injury and LPS content were significantly increased after intestinal flora imbalance or jejunum injury, and the levels of TLR signaling-related genes were significantly increased. The results indicated that Se deficiency disrupted the microbiota balance, decreased the expression of intestinal TJ factors, and increased intestinal permeability. By contrast, LPS increased due to a bacterial imbalance, which may induce inflammatory liver injury via the TLR4 signaling pathway.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2024 |
|---|---|
| Erschienen: |
2024 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:50 |
|---|---|
| Enthalten in: |
BioFactors (Oxford, England) - 50(2024), 2 vom: 08. März, Seite 311-325 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Wang, Guodong [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
Gut |
|---|
| Anmerkungen: |
Date Completed 15.04.2024 Date Revised 15.04.2024 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1002/biof.2006 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM361741154 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM361741154 | ||
| 003 | DE-627 | ||
| 005 | 20240415232918.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231226s2024 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1002/biof.2006 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n1376.xml |
| 035 | |a (DE-627)NLM361741154 | ||
| 035 | |a (NLM)37676478 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Wang, Guodong |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Gut microbiota contribution to selenium deficiency-induced gut-liver inflammation |
| 264 | 1 | |c 2024 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 15.04.2024 | ||
| 500 | |a Date Revised 15.04.2024 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a © 2023 International Union of Biochemistry and Molecular Biology. | ||
| 520 | |a There is limited knowledge about the factors that drive gut-liver axis changes after selenium (Se) deficiency-induced gut or liver injuries. Thus, we tested Se deficiency in mice to determine its effects on intestinal bacterial balance and whether it induced liver injury. Serum Se concentration, lipopolysaccharide (LPS) level, and liver injury biomarkers were tested using a biochemical method, while pathological changes in the liver and jejunum were observed via hematoxylin and eosin stain, and a fluorescence spectrophotometer was used to evaluate intestinal permeability. Tight junction (TJ)-related and toll-like receptor (TLR) signaling-related pathway genes and proteins were tested using quantitative polymerase chain reaction, western blotting, immunohistochemistry, and 16S ribosomal ribonucleic acid gene-targeted sequencing of jejunum microorganisms. Se deficiency significantly decreased glutathione peroxidase activity and disrupted the intestinal flora, with the most significant effect being a decrease in Lactobacillus reuteri. The expression of TJ-related genes and proteins decreased significantly with increased treatment time, whereas supplementation with Se, fecal microbiota transplantation, or L. reuteri reversed these decreases. Signs of liver injury and LPS content were significantly increased after intestinal flora imbalance or jejunum injury, and the levels of TLR signaling-related genes were significantly increased. The results indicated that Se deficiency disrupted the microbiota balance, decreased the expression of intestinal TJ factors, and increased intestinal permeability. By contrast, LPS increased due to a bacterial imbalance, which may induce inflammatory liver injury via the TLR4 signaling pathway | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a TLR4/MyD88/NF‐κB | |
| 650 | 4 | |a gut | |
| 650 | 4 | |a liver | |
| 650 | 4 | |a mice | |
| 650 | 4 | |a microbiota | |
| 650 | 4 | |a selenium | |
| 650 | 7 | |a Lipopolysaccharides |2 NLM | |
| 650 | 7 | |a Selenium |2 NLM | |
| 650 | 7 | |a H6241UJ22B |2 NLM | |
| 650 | 7 | |a Toll-Like Receptor 4 |2 NLM | |
| 650 | 7 | |a NF-kappa B |2 NLM | |
| 700 | 1 | |a Jiang, Zhihui |e verfasserin |4 aut | |
| 700 | 1 | |a Song, Yuwei |e verfasserin |4 aut | |
| 700 | 1 | |a Xing, Yueteng |e verfasserin |4 aut | |
| 700 | 1 | |a He, Simin |e verfasserin |4 aut | |
| 700 | 1 | |a Boomi, P |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t BioFactors (Oxford, England) |d 1989 |g 50(2024), 2 vom: 08. März, Seite 311-325 |w (DE-627)NLM01264532X |x 1872-8081 |7 nnns |
| 773 | 1 | 8 | |g volume:50 |g year:2024 |g number:2 |g day:08 |g month:03 |g pages:311-325 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1002/biof.2006 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 50 |j 2024 |e 2 |b 08 |c 03 |h 311-325 | ||