Skip to main content Deutsch

Plastic particles can increase intestinal inflammation

Study shows interaction between micro- and nanoplastics and ulcerative colitis
All News
Copyright (c) 2023 Andrzej Rostek/Shutterstock

(Vienna, 08 January 2026) A research team led by the Medical University of Vienna and the University of Vienna has investigated a possible link between the rising number of people with chronic inflammatory bowel disease and the increasing exposure to micro- and nanoplastics (MNPs). The research shows that plastic particles influence the immune cells and the intestinal microbiome and can thus increase inflammation. The results were recently published in the journal Microplastics and Nanoplastics. 

The harmful effects of MNP were investigated in a mouse model with ulcerative colitis, one of the most common forms of chronic inflammatory bowel disease. The study focussed on polystyrene particles of different sizes that were applied orally. Polystyrene is a widely used plastic that is frequently used for food packaging such as yoghurt cups, meat trays or take-away boxes. The research team's extensive molecular and histological analyses provided evidence of interactions between MNP and intestinal inflammation

The uptake of MNP by the intestinal mucosa was increased under inflammatory conditions. In addition, MNP exposure intensified the inflammatory immune response in the gut by triggering a pro-inflammatory activation of certain immune cells (macrophages). In addition, MNP exposure led to a disruption of the gut microbiome: the researchers observed a decrease in beneficial and an increase in pro-inflammatory and potentially harmful bacterial species. 

Effects beyond the intestine
"Furthermore, our study shows that under inflammatory conditions, MNPs not only accumulate in the intestine but also in other excretory organs such as the liver and kidneys, as well as in the bloodstream," explains study leader Lukas Kenner from the Medical University of Vienna. This effect was observed particularly in the case of the very small nanoplastic particles, measuring less than 0.0003 millimeters, and indicates "that MNPs can cross biological barriers and have systemic effects far beyond the intestine," adds co-study leader Verena Pichler from the University of Vienna.

Chronic inflammatory bowel diseases such as ulcerative colitis are on the rise, as is pollution from micro and nanoplastic particles. As the gastrointestinal tract is particularly exposed to increasing MNP exposure, the scientists focussed on researching a possible correlation: "Our results indicate that MNP is a previously underestimated factor in the development and intensification of chronic inflammatory bowel diseases," says Lukas Kenner. Further studies should substantiate the findings. "However, the urgent appeal to society and politicians to take measures to reduce MNP pollution is already clear."

The study was conducted in cooperation with the biomarker research institute CBMed GmbH (Graz, Austria) within the COMET module "microONE", funded by the Federal Ministry of Economy, Energy and Tourism (BMWET), the Federal Ministry of Innovation, Mobility and Infrastucture (BMIMI), Land Steiermark (Styrian Business Promotion Agency – SFG) and Land Wien (Vienna Business Agency – WAW). The COMET Module programme is executed by the Austrian Research Promotion Agency (FFG).

Publication: Microplastics and Nanoplastics
Polystyrene micro- and nanoplastics aggravates colitis in a mouse model - effects on biodistribution, macrophage polarisation and gut microbiome.
Verena Kopatz, Ulrike Resch, Kristina Draganic, Angela Horvath, Janette Pfneissl, Julijan Kabiljo, Bernadette Mödl, Gerald Timelthaler, Julia Wallner, Zeynab Mirzaei, Saule Beratlyte, Michaela Schlederer, Stefan Sarbu, Simina Laslau, Oldamur Hollóczki, Martin Raigel, Elisabeth S. Gruber, Joachim Widder, Iris Kufferath, Marion Pollheimer, Wolfgang Wadsak, George Sarau, Silke Christiansen, Nikola Zlatkov Kolev, Marcus Krueger, Robert Eferl, Gerda Egger, Vanessa Stadlbauer, Verena Pichler, Lukas Kenner.
DOI: 10.1186/s43591-025-00160-7
https://link.springer.com/article/10.1186/s43591-025-00160-7