Crohn's disease is a condition of unknown etiology with an immune-mediated pathogenesis. The subgroup of Crohn's disease with a stricturing phenotype represents a particular challenge for clinicians, as currently no effective medical therapies are available for the prevention or treatment of fibrosis. Autophagy is a key mechanism in the regulation of cellular homeostasis, and preliminary reports from our group and others have suggested a potential role in the pathogenesis of fibrostenotic complications in Crohn's disease.
The next-generation probiotic Clostridium butyricum has recently been proposed as a treatment option in several conditions, including inflammatory bowel diseases (IBD). Its beneficial effects are mainly exerted through the production of butyric acid, which in turn plays important roles at the intestinal mucosal level, including the stimulation of autophagy. The possibility of stimulating autophagy in patients with stricturing Crohn's disease may represent a promising therapeutic approach for the prevention and treatment of fibrosis.
This study involves the collection of biopsy and blood samples from 40 patients with stricturing Crohn's disease undergoing colonoscopy. In the two months preceding colonoscopy, patients will be randomized into four groups:
Patients treated with C. butyricum
Patients treated with the autophagy stimulator trehalose
Patients treated with C. butyricum + trehalose
Patients treated with placebo
Laboratory analyses will be performed on biopsy and blood samples to evaluate and quantify molecular mediators involved in inflammation, fibrosis, and autophagy.