Particulate matter 10 exposure affects intestinal functionality in both inflamed 2D intestinal epithelial cell and 3D intestinal organoid models.

absorptive function calcium signaling human intestinal epithelium human intestinal organoid inflammation particulate matter 10

Journal

Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960

Informations de publication

Date de publication:
2023
Historique:
received: 17 02 2023
accepted: 30 05 2023
medline: 13 7 2023
pubmed: 12 7 2023
entrez: 12 7 2023
Statut: epublish

Résumé

A growing body of evidence suggests that particulate matter (PM10) enters the gastrointestinal (GI) tract directly, causing the GI epithelial cells to function less efficiently, leading to inflammation and an imbalance in the gut microbiome. PM10 may, however, act as an exacerbation factor in patients with inflamed intestinal epithelium, which is associated with inflammatory bowel disease. The purpose of this study was to dissect the pathology mechanism of PM10 exposure in inflamed intestines. In this study, we established chronically inflamed intestinal epithelium models utilizing two-dimensional (2D) human intestinal epithelial cells (hIECs) and 3D human intestinal organoids (hIOs), which mimic Inflamed 2D hIECs and 3D hIOs exhibited pathological features, such as inflammation, decreased intestinal markers, and defective epithelial barrier function. In addition, we found that PM10 exposure induced a more severe disturbance of peptide uptake in inflamed 2D hIECs and 3D hIOs than in control cells. This was due to the fact that it interferes with calcium signaling, protein digestion, and absorption pathways. The findings demonstrate that PM10-induced epithelial alterations contribute to the exacerbation of inflammatory disorders caused by the intestine. According to our findings, 2D hIEC and 3D hIO models could be powerful

Sections du résumé

Background
A growing body of evidence suggests that particulate matter (PM10) enters the gastrointestinal (GI) tract directly, causing the GI epithelial cells to function less efficiently, leading to inflammation and an imbalance in the gut microbiome. PM10 may, however, act as an exacerbation factor in patients with inflamed intestinal epithelium, which is associated with inflammatory bowel disease.
Objective
The purpose of this study was to dissect the pathology mechanism of PM10 exposure in inflamed intestines.
Methods
In this study, we established chronically inflamed intestinal epithelium models utilizing two-dimensional (2D) human intestinal epithelial cells (hIECs) and 3D human intestinal organoids (hIOs), which mimic
Results
Inflamed 2D hIECs and 3D hIOs exhibited pathological features, such as inflammation, decreased intestinal markers, and defective epithelial barrier function. In addition, we found that PM10 exposure induced a more severe disturbance of peptide uptake in inflamed 2D hIECs and 3D hIOs than in control cells. This was due to the fact that it interferes with calcium signaling, protein digestion, and absorption pathways. The findings demonstrate that PM10-induced epithelial alterations contribute to the exacerbation of inflammatory disorders caused by the intestine.
Conclusions
According to our findings, 2D hIEC and 3D hIO models could be powerful

Identifiants

pubmed: 37435069
doi: 10.3389/fimmu.2023.1168064
pmc: PMC10331606
doi:

Substances chimiques

Particulate Matter 0

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

1168064

Informations de copyright

Copyright © 2023 Son, Son, Yu, Baek, Park, Lee, Lee, Kim and Son.

Déclaration de conflit d'intérêts

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

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Auteurs

Ye Seul Son (YS)

Department of Stem Cell Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.

Naeun Son (N)

Department of Stem Cell Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.
Department of Bio-Molecular Science, Korea Research Institute of Bioscience and Biotechnology (KRIBB) School of Bioscience, University of Science and Technology (UST), Daejeon, Republic of Korea.

Won Dong Yu (WD)

Department of Stem Cell Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.
Department of Bio-Molecular Science, Korea Research Institute of Bioscience and Biotechnology (KRIBB) School of Bioscience, University of Science and Technology (UST), Daejeon, Republic of Korea.

Aruem Baek (A)

Department of Stem Cell Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.

Young-Jun Park (YJ)

Environmental Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.

Moo-Seung Lee (MS)

Environmental Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.

Seon-Jin Lee (SJ)

Environmental Disease Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.

Dae-Soo Kim (DS)

Digital Biotech Innovation Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.

Mi-Young Son (MY)

Department of Stem Cell Convergence Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Daejeon, Republic of Korea.
Department of Bio-Molecular Science, Korea Research Institute of Bioscience and Biotechnology (KRIBB) School of Bioscience, University of Science and Technology (UST), Daejeon, Republic of Korea.

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