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Kefir peptides attenuate intestinal injury induced by combined exposure to microplastics and particulate matter
Tsai-Chun Lai1, Chuan-Mu Chen2
1Department of Life Sciences, College of Life Sciences, National Chung Hsing University, Taichung 402202, Taiwan; The iEGG and Animal Biotechnology Center, National Chung Hsing University, Taichung 402202, Taiwan; Department of Post-Baccalaureate Medicine, National Chung Hsing University, Taichung 402202, Taiwan.
Abstract:
Microplastics (MP) and particulate matter (PM) are pervasive environmental contaminants that pose significant threats to intestinal homeostasis. This study systematically investigated the individual and combined effects of MP and PM on intestinal injury using complementary in vivo and in vitro models. In mice, co-exposure to MP and PM induced pronounced oxidative stress, intestinal inflammation, disruption of epithelial barrier integrity, mucin accumulation, activation of endoplasmic reticulum (ER) stress, and dysregulation of autophagy. Consistently, in C2BBe1 intestinal epithelial cells, combined exposure significantly reduced cell viability and exacerbated oxidative stress, ER stress, and autophagic imbalance, as evidenced by increased reactive oxygen species (ROS), elevated BiP and ATF6 expression, and accumulation of p62 and LC3B-II. Moreover, co-exposure promoted intestinal inflammation, barrier dysfunction, and mucin accumulation, demonstrated by increased ICAM-1, IL-1β, IL-6, and TNFα levels, reduced ZO-1 expression, and upregulated MUC2 expression. Strikingly, combined exposure-induced mucin accumulation may provide physical protection and compensate for barrier disruption. Notably, pretreatment with kefir peptides (KPs) markedly attenuated these deleterious effects in vivo and in vitro, supporting their protective potential. KPs pretreatment alleviated cytotoxicity by reducing oxidative and ER stress markers and normalizing autophagy-related protein expression. In addition, KPs decreased ICAM-1 levels, restored epithelial barrier integrity, and limited mucin accumulation in intestinal cells. Collectively, these findings demonstrate that concurrent exposure to MP and PM exacerbates intestinal injury through coordinated activation of oxidative stress, ER stress, and dysregulated autophagy pathways, and identify KPs as a promising preventive strategy for mitigating pollutant-induced intestinal damage.
Insights
Combined exposure to microplastics (MP) and particulate matter (PM) causes significant intestinal injury by increasing oxidative stress and inflammation. Kefir peptides (KPs) show promise in preventing this damage.
Area of Science:
- Environmental Health
- Toxicology
- Gastroenterology
Background:
- Microplastics (MP) and particulate matter (PM) are widespread environmental contaminants.
- These pollutants pose risks to intestinal homeostasis and overall health.
Purpose of the Study:
- To investigate the combined effects of MP and PM on intestinal injury.
- To evaluate the protective potential of kefir peptides (KPs) against MP and PM-induced intestinal damage.
Main Methods:
- Utilized complementary in vivo (mice) and in vitro (C2BBe1 intestinal cells) models.
- Assessed oxidative stress, inflammation, epithelial barrier integrity, endoplasmic reticulum (ER) stress, and autophagy.
- Measured levels of reactive oxygen species (ROS), inflammatory cytokines, barrier proteins (ZO-1), mucin (MUC2), and autophagy markers (p62, LC3B-II).
Main Results:
- Co-exposure to MP and PM induced significant oxidative stress, ER stress, inflammation, and barrier dysfunction in the intestine.
- These pollutants dysregulated autophagy pathways and increased mucin accumulation.
- Kefir peptides (KPs) pretreatment effectively attenuated MP and PM-induced cytotoxicity, oxidative stress, ER stress, and inflammation, while restoring barrier integrity.
Conclusions:
- Concurrent exposure to MP and PM exacerbates intestinal injury via coordinated activation of oxidative stress, ER stress, and autophagy pathways.
- Kefir peptides (KPs) represent a potential preventive strategy for mitigating pollutant-induced intestinal damage.
