What is it about?
This study looked at tiny particles called membrane vesicles that are naturally released by the bacterium Clostridioides difficile. We tested whether these vesicles could change the normal behavior of colon cells. Using both cell cultures and mice, we found that vesicles from some strains, especially ribotype RT084, can activate a process called epithelial-mesenchymal transition (EMT). EMT makes epithelial cells lose their normal structure and take on features linked to cancer development and tissue damage. The results suggest that these bacterial vesicles may contribute to harmful changes in the gut and could be involved in the early steps of colon disease, including cancer.
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Why is it important?
Clostridioides difficile is best known for causing diarrhea through its toxins, but this work shows that other bacterial products, like vesicles, may also damage the gut and drive cancer-related processes. Understanding this new mechanism is important because it highlights how infections could influence long-term colon health, not just short-term illness. It also opens the door to exploring vesicles as potential tools for vaccines, diagnostics, or drug delivery systems.
Perspectives
From my perspective, this work is exciting because it expands our understanding of C. difficile beyond its well-known toxins. By showing that bacterial vesicles alone can trigger cancer-related changes, it suggests we may need to rethink how we approach gut infections and their long-term consequences. It also raises interesting questions about whether we could turn these vesicles into something useful—such as new therapeutic platforms or preventive strategies against C. difficile.
Professor Stefano Di Bella
Universita degli Studi di Trieste
Read the Original
This page is a summary of: Membrane vesicles from selected Clostridioides difficile strains induce epithelial-mesenchymal transition in colonic epithelial cells: insights from in vitro and in vivo studies, Microbial Pathogenesis, November 2025, Elsevier,
DOI: 10.1016/j.micpath.2025.107988.
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