Vitamin A inhibits the action of LPS on the intestinal epithelial barrier function and tight junction proteins
Inflammation caused by either intrinsic or extrinsic toxins results in intestinal barrier dysfunction, contributing to inflammatory bowel disease (IBD) and other diseases. Vitamin A is a widely used food supplement although its mechanistic effect on intestinal structures is largely unknown. The goal...
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| Published in | Food & function Vol. 10; no. 2; pp. 1235 - 1242 |
|---|---|
| Main Authors | , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
England
Royal Society of Chemistry
20.02.2019
|
| Subjects | |
| Online Access | Get full text |
| ISSN | 2042-6496 2042-650X 2042-650X |
| DOI | 10.1039/C8FO01123K |
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| Abstract | Inflammation caused by either intrinsic or extrinsic toxins results in intestinal barrier dysfunction, contributing to inflammatory bowel disease (IBD) and other diseases. Vitamin A is a widely used food supplement although its mechanistic effect on intestinal structures is largely unknown. The goal of this study was to explore the mechanism by investigating the influence of vitamin A on the intestinal barrier function, represented by tight junctions. IPEC-J2 cells were differentiated on transwell inserts and used as a model of intestinal barrier permeability. Transepithelial electrical resistance (TEER) was used as an indicator of monolayer integrity and paracellular permeability. Western blot and the reverse transcriptase-polymerase chain reaction were used to assess the protein and mRNA expression of tight junction proteins. Immunofluorescence microscopy was used to evaluate the localization and expression of tight junctions. Differentiated cells were treated with a vehicle control (Ctrl), inflammatory stimulus (1 μg mL
−1
LPS), LPS co-treatment with 0.1 μmol L
−1
Vitamin A (1 μg mL
−1
LPS + 0.1 μmol L
−1
VA) and 0.1 μmol L
−1
Vitamin A. LPS significantly decreased TEER by 24 hours, continuing this effect to 48 hours after application. Vitamin A alleviated the LPS-induced decrease of TEER from 12 hours to 48 hours, while Vitamin A alone enhanced TEER, indicating that Vitamin A attenuated LPS-induced intestinal epithelium permeability. Mechanistically, different concentrations of Vitamin A (0–20 μmol L
−1
) enhanced tight junction protein markers including Zo-1, Occludin and Claudin-1 both at protein and mRNA levels with an optimized dose of 0.1 μmol L
−1
. Immunofluorescence results demonstrated that majority of Zo-1 and Claudin-1 is located at the tight junctions, as we expected. LPS reduced the expression of these proteins and Vitamin A reversed LPS-reduced expression of these proteins, consistent with the results of western blot. In conclusion, Vitamin A improves the intestinal barrier function and reverses LPS-induced intestinal barrier damage
via
enhancing the expression of tight junction proteins. |
|---|---|
| AbstractList | Inflammation caused by either intrinsic or extrinsic toxins results in intestinal barrier dysfunction, contributing to inflammatory bowel disease (IBD) and other diseases. Vitamin A is a widely used food supplement although its mechanistic effect on intestinal structures is largely unknown. The goal of this study was to explore the mechanism by investigating the influence of vitamin A on the intestinal barrier function, represented by tight junctions. IPEC-J2 cells were differentiated on transwell inserts and used as a model of intestinal barrier permeability. Transepithelial electrical resistance (TEER) was used as an indicator of monolayer integrity and paracellular permeability. Western blot and the reverse transcriptase-polymerase chain reaction were used to assess the protein and mRNA expression of tight junction proteins. Immunofluorescence microscopy was used to evaluate the localization and expression of tight junctions. Differentiated cells were treated with a vehicle control (Ctrl), inflammatory stimulus (1 μg mL
−1
LPS), LPS co-treatment with 0.1 μmol L
−1
Vitamin A (1 μg mL
−1
LPS + 0.1 μmol L
−1
VA) and 0.1 μmol L
−1
Vitamin A. LPS significantly decreased TEER by 24 hours, continuing this effect to 48 hours after application. Vitamin A alleviated the LPS-induced decrease of TEER from 12 hours to 48 hours, while Vitamin A alone enhanced TEER, indicating that Vitamin A attenuated LPS-induced intestinal epithelium permeability. Mechanistically, different concentrations of Vitamin A (0–20 μmol L
−1
) enhanced tight junction protein markers including Zo-1, Occludin and Claudin-1 both at protein and mRNA levels with an optimized dose of 0.1 μmol L
−1
. Immunofluorescence results demonstrated that majority of Zo-1 and Claudin-1 is located at the tight junctions, as we expected. LPS reduced the expression of these proteins and Vitamin A reversed LPS-reduced expression of these proteins, consistent with the results of western blot. In conclusion, Vitamin A improves the intestinal barrier function and reverses LPS-induced intestinal barrier damage
via
enhancing the expression of tight junction proteins. Inflammation caused by either intrinsic or extrinsic toxins results in intestinal barrier dysfunction, contributing to inflammatory bowel disease (IBD) and other diseases. Vitamin A is a widely used food supplement although its mechanistic effect on intestinal structures is largely unknown. The goal of this study was to explore the mechanism by investigating the influence of vitamin A on the intestinal barrier function, represented by tight junctions. IPEC-J2 cells were differentiated on transwell inserts and used as a model of intestinal barrier permeability. Transepithelial electrical resistance (TEER) was used as an indicator of monolayer integrity and paracellular permeability. Western blot and the reverse transcriptase-polymerase chain reaction were used to assess the protein and mRNA expression of tight junction proteins. Immunofluorescence microscopy was used to evaluate the localization and expression of tight junctions. Differentiated cells were treated with a vehicle control (Ctrl), inflammatory stimulus (1 μg mL⁻¹ LPS), LPS co-treatment with 0.1 μmol L⁻¹ Vitamin A (1 μg mL⁻¹ LPS + 0.1 μmol L⁻¹ VA) and 0.1 μmol L⁻¹ Vitamin A. LPS significantly decreased TEER by 24 hours, continuing this effect to 48 hours after application. Vitamin A alleviated the LPS-induced decrease of TEER from 12 hours to 48 hours, while Vitamin A alone enhanced TEER, indicating that Vitamin A attenuated LPS-induced intestinal epithelium permeability. Mechanistically, different concentrations of Vitamin A (0–20 μmol L⁻¹) enhanced tight junction protein markers including Zo-1, Occludin and Claudin-1 both at protein and mRNA levels with an optimized dose of 0.1 μmol L⁻¹. Immunofluorescence results demonstrated that majority of Zo-1 and Claudin-1 is located at the tight junctions, as we expected. LPS reduced the expression of these proteins and Vitamin A reversed LPS-reduced expression of these proteins, consistent with the results of western blot. In conclusion, Vitamin A improves the intestinal barrier function and reverses LPS-induced intestinal barrier damage via enhancing the expression of tight junction proteins. Inflammation caused by either intrinsic or extrinsic toxins results in intestinal barrier dysfunction, contributing to inflammatory bowel disease (IBD) and other diseases. Vitamin A is a widely used food supplement although its mechanistic effect on intestinal structures is largely unknown. The goal of this study was to explore the mechanism by investigating the influence of vitamin A on the intestinal barrier function, represented by tight junctions. IPEC-J2 cells were differentiated on transwell inserts and used as a model of intestinal barrier permeability. Transepithelial electrical resistance (TEER) was used as an indicator of monolayer integrity and paracellular permeability. Western blot and the reverse transcriptase-polymerase chain reaction were used to assess the protein and mRNA expression of tight junction proteins. Immunofluorescence microscopy was used to evaluate the localization and expression of tight junctions. Differentiated cells were treated with a vehicle control (Ctrl), inflammatory stimulus (1 μg mL-1 LPS), LPS co-treatment with 0.1 μmol L-1 Vitamin A (1 μg mL-1 LPS + 0.1 μmol L-1 VA) and 0.1 μmol L-1 Vitamin A. LPS significantly decreased TEER by 24 hours, continuing this effect to 48 hours after application. Vitamin A alleviated the LPS-induced decrease of TEER from 12 hours to 48 hours, while Vitamin A alone enhanced TEER, indicating that Vitamin A attenuated LPS-induced intestinal epithelium permeability. Mechanistically, different concentrations of Vitamin A (0-20 μmol L-1) enhanced tight junction protein markers including Zo-1, Occludin and Claudin-1 both at protein and mRNA levels with an optimized dose of 0.1 μmol L-1. Immunofluorescence results demonstrated that majority of Zo-1 and Claudin-1 is located at the tight junctions, as we expected. LPS reduced the expression of these proteins and Vitamin A reversed LPS-reduced expression of these proteins, consistent with the results of western blot. In conclusion, Vitamin A improves the intestinal barrier function and reverses LPS-induced intestinal barrier damage via enhancing the expression of tight junction proteins. Inflammation caused by either intrinsic or extrinsic toxins results in intestinal barrier dysfunction, contributing to inflammatory bowel disease (IBD) and other diseases. Vitamin A is a widely used food supplement although its mechanistic effect on intestinal structures is largely unknown. The goal of this study was to explore the mechanism by investigating the influence of vitamin A on the intestinal barrier function, represented by tight junctions. IPEC-J2 cells were differentiated on transwell inserts and used as a model of intestinal barrier permeability. Transepithelial electrical resistance (TEER) was used as an indicator of monolayer integrity and paracellular permeability. Western blot and the reverse transcriptase-polymerase chain reaction were used to assess the protein and mRNA expression of tight junction proteins. Immunofluorescence microscopy was used to evaluate the localization and expression of tight junctions. Differentiated cells were treated with a vehicle control (Ctrl), inflammatory stimulus (1 μg mL−1 LPS), LPS co-treatment with 0.1 μmol L−1 Vitamin A (1 μg mL−1 LPS + 0.1 μmol L−1 VA) and 0.1 μmol L−1 Vitamin A. LPS significantly decreased TEER by 24 hours, continuing this effect to 48 hours after application. Vitamin A alleviated the LPS-induced decrease of TEER from 12 hours to 48 hours, while Vitamin A alone enhanced TEER, indicating that Vitamin A attenuated LPS-induced intestinal epithelium permeability. Mechanistically, different concentrations of Vitamin A (0–20 μmol L−1) enhanced tight junction protein markers including Zo-1, Occludin and Claudin-1 both at protein and mRNA levels with an optimized dose of 0.1 μmol L−1. Immunofluorescence results demonstrated that majority of Zo-1 and Claudin-1 is located at the tight junctions, as we expected. LPS reduced the expression of these proteins and Vitamin A reversed LPS-reduced expression of these proteins, consistent with the results of western blot. In conclusion, Vitamin A improves the intestinal barrier function and reverses LPS-induced intestinal barrier damage via enhancing the expression of tight junction proteins. Inflammation caused by either intrinsic or extrinsic toxins results in intestinal barrier dysfunction, contributing to inflammatory bowel disease (IBD) and other diseases. Vitamin A is a widely used food supplement although its mechanistic effect on intestinal structures is largely unknown. The goal of this study was to explore the mechanism by investigating the influence of vitamin A on the intestinal barrier function, represented by tight junctions. IPEC-J2 cells were differentiated on transwell inserts and used as a model of intestinal barrier permeability. Transepithelial electrical resistance (TEER) was used as an indicator of monolayer integrity and paracellular permeability. Western blot and the reverse transcriptase-polymerase chain reaction were used to assess the protein and mRNA expression of tight junction proteins. Immunofluorescence microscopy was used to evaluate the localization and expression of tight junctions. Differentiated cells were treated with a vehicle control (Ctrl), inflammatory stimulus (1 μg mL-1 LPS), LPS co-treatment with 0.1 μmol L-1 Vitamin A (1 μg mL-1 LPS + 0.1 μmol L-1 VA) and 0.1 μmol L-1 Vitamin A. LPS significantly decreased TEER by 24 hours, continuing this effect to 48 hours after application. Vitamin A alleviated the LPS-induced decrease of TEER from 12 hours to 48 hours, while Vitamin A alone enhanced TEER, indicating that Vitamin A attenuated LPS-induced intestinal epithelium permeability. Mechanistically, different concentrations of Vitamin A (0-20 μmol L-1) enhanced tight junction protein markers including Zo-1, Occludin and Claudin-1 both at protein and mRNA levels with an optimized dose of 0.1 μmol L-1. Immunofluorescence results demonstrated that majority of Zo-1 and Claudin-1 is located at the tight junctions, as we expected. LPS reduced the expression of these proteins and Vitamin A reversed LPS-reduced expression of these proteins, consistent with the results of western blot. In conclusion, Vitamin A improves the intestinal barrier function and reverses LPS-induced intestinal barrier damage via enhancing the expression of tight junction proteins.Inflammation caused by either intrinsic or extrinsic toxins results in intestinal barrier dysfunction, contributing to inflammatory bowel disease (IBD) and other diseases. Vitamin A is a widely used food supplement although its mechanistic effect on intestinal structures is largely unknown. The goal of this study was to explore the mechanism by investigating the influence of vitamin A on the intestinal barrier function, represented by tight junctions. IPEC-J2 cells were differentiated on transwell inserts and used as a model of intestinal barrier permeability. Transepithelial electrical resistance (TEER) was used as an indicator of monolayer integrity and paracellular permeability. Western blot and the reverse transcriptase-polymerase chain reaction were used to assess the protein and mRNA expression of tight junction proteins. Immunofluorescence microscopy was used to evaluate the localization and expression of tight junctions. Differentiated cells were treated with a vehicle control (Ctrl), inflammatory stimulus (1 μg mL-1 LPS), LPS co-treatment with 0.1 μmol L-1 Vitamin A (1 μg mL-1 LPS + 0.1 μmol L-1 VA) and 0.1 μmol L-1 Vitamin A. LPS significantly decreased TEER by 24 hours, continuing this effect to 48 hours after application. Vitamin A alleviated the LPS-induced decrease of TEER from 12 hours to 48 hours, while Vitamin A alone enhanced TEER, indicating that Vitamin A attenuated LPS-induced intestinal epithelium permeability. Mechanistically, different concentrations of Vitamin A (0-20 μmol L-1) enhanced tight junction protein markers including Zo-1, Occludin and Claudin-1 both at protein and mRNA levels with an optimized dose of 0.1 μmol L-1. Immunofluorescence results demonstrated that majority of Zo-1 and Claudin-1 is located at the tight junctions, as we expected. LPS reduced the expression of these proteins and Vitamin A reversed LPS-reduced expression of these proteins, consistent with the results of western blot. In conclusion, Vitamin A improves the intestinal barrier function and reverses LPS-induced intestinal barrier damage via enhancing the expression of tight junction proteins. |
| Author | Huang, Yanjun Wu, Jingtao Zhou, Sichun Xiao, Di Darko, Kwame Oteng Deng, Jun Yang, Xiaoping He, Caimei Peng, Mei Tao, Ting Hu, Xin Wang, Zhiren |
| Author_xml | – sequence: 1 givenname: Caimei surname: He fullname: He, Caimei organization: Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha – sequence: 2 givenname: Jun surname: Deng fullname: Deng, Jun organization: Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha – sequence: 3 givenname: Xin surname: Hu fullname: Hu, Xin organization: Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha – sequence: 4 givenname: Sichun surname: Zhou fullname: Zhou, Sichun organization: Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha – sequence: 5 givenname: Jingtao surname: Wu fullname: Wu, Jingtao organization: Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha – sequence: 6 givenname: Di surname: Xiao fullname: Xiao, Di organization: Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha – sequence: 7 givenname: Kwame Oteng surname: Darko fullname: Darko, Kwame Oteng organization: Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha – sequence: 8 givenname: Yanjun surname: Huang fullname: Huang, Yanjun organization: Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha – sequence: 9 givenname: Ting surname: Tao fullname: Tao, Ting organization: Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha – sequence: 10 givenname: Mei surname: Peng fullname: Peng, Mei organization: Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha – sequence: 11 givenname: Zhiren orcidid: 0000-0002-2016-0517 surname: Wang fullname: Wang, Zhiren organization: Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha – sequence: 12 givenname: Xiaoping orcidid: 0000-0003-1952-7227 surname: Yang fullname: Yang, Xiaoping organization: Key Laboratory of Study and Discovery of Small Targeted Molecules of Hunan Province, Department of Pharmacy, School of Medicine, Hunan Normal University, Changsha |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/30747184$$D View this record in MEDLINE/PubMed |
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| Snippet | Inflammation caused by either intrinsic or extrinsic toxins results in intestinal barrier dysfunction, contributing to inflammatory bowel disease (IBD) and... |
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| SubjectTerms | Barriers Dietary supplements Electrical junctions electrical resistance Epithelium fluorescence microscopy fluorescent antibody technique Gene expression Immunofluorescence inflammation inflammatory bowel disease Inflammatory bowel diseases Inserts intestinal mucosa Intestine Lipopolysaccharides Localization Membrane permeability messenger RNA occludins Permeability Polymerase chain reaction Proteins reverse transcriptase polymerase chain reaction RNA-directed DNA polymerase Tight junctions Toxins Vitamin A Western blotting Zonula occludens-1 protein |
| Title | Vitamin A inhibits the action of LPS on the intestinal epithelial barrier function and tight junction proteins |
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