Hypothesized Mechanisms by Which Chronic Clostridioides difficile Infection May Promote Colorectal Tumorigenesis (IMAGE)
Caption
This graphical abstract illustrates the emerging concept that chronic Clostridioides difficile (C. difficile) infection may function as a previously unrecognized pro-carcinogenic driver in gastrointestinal tumors, particularly colorectal cancer (CRC). Experimental evidence suggests that C. difficile-induced gut dysbiosis, persistent toxin exposure (TcdA, TcdB, CDT), and host–microbe interactions collectively contribute to colonic tumorigenic processes. The proposed etiological mechanisms include epithelial injury, cellular senescence, oxidative stress, metabolic reprogramming, biofilm formation, virulence factor activity, and immune evasion, which together amplify proinflammatory signaling and microenvironmental changes that favor CRC initiation and progression. This model highlights the potential significance of C. difficile as a biomarker and pathogenic contributor to CRC, providing new insights for preventing tumorigenesis, recurrence, and metastasis.
Credit
Ju Zou, a PhD student from Xiangya Hospital Central South University
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Credit must be given to the creator. Only noncommercial uses of the work are permitted. No derivatives or adaptations of the work are permitted.
License
CC BY-NC-ND