» Articles » PMID: 37435069

Particulate Matter 10 Exposure Affects Intestinal Functionality in Both Inflamed 2D Intestinal Epithelial Cell and 3D Intestinal Organoid Models

Overview
Journal Front Immunol
Date 2023 Jul 12
PMID 37435069
Authors
Affiliations
Soon will be listed here.
Abstract

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 cellular diversity and function, in order to examine the deleterious effects of PM10 in human intestine-like models.

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 platforms for the evaluation of the causal relationship between PM exposure and abnormal human intestinal functions.

Citing Articles

Long-term exposure to air pollution and gastrointestinal disease: findings from a nationwide cohort study in China.

Kou Y, Ye S, Du W, Lu Z, Yang K, Zhan L BMC Public Health. 2025; 25(1):1011.

PMID: 40087627 DOI: 10.1186/s12889-025-21910-5.


Emerging role of environmental pollutants in inflammatory bowel disease risk, outcomes and underlying mechanisms.

Estevinho M, Midya V, Cohen-Mekelburg S, Allin K, Fumery M, Pinho S Gut. 2024; 74(3):477-486.

PMID: 39179372 PMC: 11802320. DOI: 10.1136/gutjnl-2024-332523.


Pollutants, microbiota and immune system: frenemies within the gut.

Rio P, Gasbarrini A, Gambassi G, Cianci R Front Public Health. 2024; 12:1285186.

PMID: 38799688 PMC: 11116734. DOI: 10.3389/fpubh.2024.1285186.

References
1.
Behrens I, Kamm W, Dantzig A, Kissel T . Variation of peptide transporter (PepT1 and HPT1) expression in Caco-2 cells as a function of cell origin. J Pharm Sci. 2004; 93(7):1743-54. DOI: 10.1002/jps.20062. View

2.
Putt K, Pei R, White H, Bolling B . Yogurt inhibits intestinal barrier dysfunction in Caco-2 cells by increasing tight junctions. Food Funct. 2017; 8(1):406-414. DOI: 10.1039/c6fo01592a. View

3.
Samak G, Narayanan D, Jaggar J, Rao R . CaV1.3 channels and intracellular calcium mediate osmotic stress-induced N-terminal c-Jun kinase activation and disruption of tight junctions in Caco-2 CELL MONOLAYERS. J Biol Chem. 2011; 286(34):30232-43. PMC: 3191062. DOI: 10.1074/jbc.M111.240358. View

4.
Ananthakrishnan A, McGinley E, Binion D, Saeian K . Ambient air pollution correlates with hospitalizations for inflammatory bowel disease: an ecologic analysis. Inflamm Bowel Dis. 2010; 17(5):1138-45. DOI: 10.1002/ibd.21455. View

5.
Balakrishnan K, Cohen A, Smith K . Addressing the burden of disease attributable to air pollution in India: the need to integrate across household and ambient air pollution exposures. Environ Health Perspect. 2014; 122(1):A6-7. PMC: 3888581. DOI: 10.1289/ehp.1307822. View