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Kefir peptides attenuate intestinal injury induced by combined exposure to microplastics and particulate matter
Summary
Microplastics and air pollution particles are everywhere, and this study found that when they team up in the gut, they cause real damage — triggering inflammation, stress on cells, and a breakdown of the gut's protective lining. The good news: peptides from kefir (a fermented milk drink) helped protect against this damage in mice and lab-grown intestinal cells, hinting that something as simple as a fermented food compound could help shield our gut from everyday pollution exposure. More research is needed before this becomes a real-world recommendation, but it's a promising lead for protecting gut health in our increasingly polluted world.
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.