In Experiment 2, the IsoLoop model effectively replicated CDI dynamics in group 2a, with infected loops showing epithelial damage, crypt necrosis, ulceration, and abscess formation, alongside robust upregulation of inflammatory pathways, including MAPK, TNF, PI3K-Akt, and chemokine signaling, recapitulating C. difficile toxin-mediated pathology.62 This evidence concerns the gene TNF and clostridium difficile infection.