Investigates inflammation mechanisms contributing to post-operative recurrence in Crohn’s disease, suggesting targets for intervention.
Despite advances in guideline-directed surveillance and initiation of biologic therapy after ileocecal resection for Crohn’s disease, many patients still experience post-operative recurrence. There is a growing field of research on the mechanisms of inflammation that are specific to post-operative recurrence after surgical resection and anastomosis. Within the innate immune system, certain genetic risk factors and an imbalance in matrix metalloproteinases have been implicated; however, the roles of specific innate immune cells are still being studied. Within the adaptive immune system, increased T-cell clonal expansion at the time of surgery and specific antibodies may play important roles in inflammation after resection. There are emerging associations to link mitochondrial oxidative stress, specific chemokines and cytokines, and microbial dysbiosis to the processes driving post-operative inflammation.
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Greenwood et al. (2026) studied this question.
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