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Butyric Acid Added Apically to Intestinal Caco-2 Cells Elevates Hepatic ApoA-I Transcription and Rescues Lower ApoA-I Expression in Inflamed HepG2 Cells Co-Cultured in the Basolateral Compartment

Apolipoprotein A-I (ApoA-I) concentrations are decreased during inflammation, which may reduce high-density lipoprotein (HDL) functionality. Thus, rescuing ApoA-I concentrations during inflammation might help to prevent atherosclerosis. Recent studies have shown that butyric acid (C4) has anti-infla...

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Autores principales: Tayyeb, Jehad Z., Popeijus, Herman E., Mensink, Ronald P., Plat, Jogchum
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7825706/
https://www.ncbi.nlm.nih.gov/pubmed/33430253
http://dx.doi.org/10.3390/biom11010071
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author Tayyeb, Jehad Z.
Popeijus, Herman E.
Mensink, Ronald P.
Plat, Jogchum
author_facet Tayyeb, Jehad Z.
Popeijus, Herman E.
Mensink, Ronald P.
Plat, Jogchum
author_sort Tayyeb, Jehad Z.
collection PubMed
description Apolipoprotein A-I (ApoA-I) concentrations are decreased during inflammation, which may reduce high-density lipoprotein (HDL) functionality. Thus, rescuing ApoA-I concentrations during inflammation might help to prevent atherosclerosis. Recent studies have shown that butyric acid (C4) has anti-inflammatory effects and rescues ApoA-I production. However, whether intestinal short chain fatty acids (SCFAs) are able to influence hepatic processes is unknown. Therefore, we investigated C4 anti-inflammatory effects on ApoA-I transcription in the intestine-liver co-culture model. C4 dose-response experiments in the presence or absence of cytokines were performed in a co-culture system including Caco-2 cells, HepG2 cells, or both. Changes in ApoA-I transcription in Caco-2 cells and HepG2 cells were analyzed using qPCR. C4 increased ApoA-I expression in HepG2 cells that cultured alone. When both cells were cultured together, C4 decreased ApoA-I expression in Caco-2 cells and increased ApoA-I expression in HepG2 cells. However, adding C4 to apical Caco-2 cells resulted in a smaller effect in HepG2 cells compared with adding C4 directly to the hepatocytes. Moreover, C4 rescued ApoA-I expression in inflamed HepG2 cells. These findings suggests that intestinal SCFAs can affect hepatic processes. However, the smaller effect in the co-culture experiment indicates cross-talk between intestine and liver.
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spelling pubmed-78257062021-01-24 Butyric Acid Added Apically to Intestinal Caco-2 Cells Elevates Hepatic ApoA-I Transcription and Rescues Lower ApoA-I Expression in Inflamed HepG2 Cells Co-Cultured in the Basolateral Compartment Tayyeb, Jehad Z. Popeijus, Herman E. Mensink, Ronald P. Plat, Jogchum Biomolecules Article Apolipoprotein A-I (ApoA-I) concentrations are decreased during inflammation, which may reduce high-density lipoprotein (HDL) functionality. Thus, rescuing ApoA-I concentrations during inflammation might help to prevent atherosclerosis. Recent studies have shown that butyric acid (C4) has anti-inflammatory effects and rescues ApoA-I production. However, whether intestinal short chain fatty acids (SCFAs) are able to influence hepatic processes is unknown. Therefore, we investigated C4 anti-inflammatory effects on ApoA-I transcription in the intestine-liver co-culture model. C4 dose-response experiments in the presence or absence of cytokines were performed in a co-culture system including Caco-2 cells, HepG2 cells, or both. Changes in ApoA-I transcription in Caco-2 cells and HepG2 cells were analyzed using qPCR. C4 increased ApoA-I expression in HepG2 cells that cultured alone. When both cells were cultured together, C4 decreased ApoA-I expression in Caco-2 cells and increased ApoA-I expression in HepG2 cells. However, adding C4 to apical Caco-2 cells resulted in a smaller effect in HepG2 cells compared with adding C4 directly to the hepatocytes. Moreover, C4 rescued ApoA-I expression in inflamed HepG2 cells. These findings suggests that intestinal SCFAs can affect hepatic processes. However, the smaller effect in the co-culture experiment indicates cross-talk between intestine and liver. MDPI 2021-01-07 /pmc/articles/PMC7825706/ /pubmed/33430253 http://dx.doi.org/10.3390/biom11010071 Text en © 2021 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Tayyeb, Jehad Z.
Popeijus, Herman E.
Mensink, Ronald P.
Plat, Jogchum
Butyric Acid Added Apically to Intestinal Caco-2 Cells Elevates Hepatic ApoA-I Transcription and Rescues Lower ApoA-I Expression in Inflamed HepG2 Cells Co-Cultured in the Basolateral Compartment
title Butyric Acid Added Apically to Intestinal Caco-2 Cells Elevates Hepatic ApoA-I Transcription and Rescues Lower ApoA-I Expression in Inflamed HepG2 Cells Co-Cultured in the Basolateral Compartment
title_full Butyric Acid Added Apically to Intestinal Caco-2 Cells Elevates Hepatic ApoA-I Transcription and Rescues Lower ApoA-I Expression in Inflamed HepG2 Cells Co-Cultured in the Basolateral Compartment
title_fullStr Butyric Acid Added Apically to Intestinal Caco-2 Cells Elevates Hepatic ApoA-I Transcription and Rescues Lower ApoA-I Expression in Inflamed HepG2 Cells Co-Cultured in the Basolateral Compartment
title_full_unstemmed Butyric Acid Added Apically to Intestinal Caco-2 Cells Elevates Hepatic ApoA-I Transcription and Rescues Lower ApoA-I Expression in Inflamed HepG2 Cells Co-Cultured in the Basolateral Compartment
title_short Butyric Acid Added Apically to Intestinal Caco-2 Cells Elevates Hepatic ApoA-I Transcription and Rescues Lower ApoA-I Expression in Inflamed HepG2 Cells Co-Cultured in the Basolateral Compartment
title_sort butyric acid added apically to intestinal caco-2 cells elevates hepatic apoa-i transcription and rescues lower apoa-i expression in inflamed hepg2 cells co-cultured in the basolateral compartment
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7825706/
https://www.ncbi.nlm.nih.gov/pubmed/33430253
http://dx.doi.org/10.3390/biom11010071
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