During the 13th Probiotics, Prebiotics and New Foods Congress, Microbiomepost.com conducted an exclusive interview with Federica Facciotti, from University of Milano Bicocca, in order to discuss how in recent years, research has increasingly focused on how the gut microbiota interacts with immune activation, shaping both chronic inflammatory intestinal disorders—such as Crohn’s disease and ulcerative colitis—and oncology, particularly colorectal cancer. 

This interview highlights a key concept: the same biological “coin” can show opposite faces depending on the clinical context. In colorectal cancer, the presence of selected microorganisms (including Fusobacterium nucleatum and Porphyromonas gingivalis) within tumor-associated mucosal microbiota and even intratumoral niches is linked to local immune suppression, with these bacteria described as directly dampening cytotoxic immune functions within the tumor microenvironment. In inflammatory bowel diseases, by contrast, microbiota composition—and especially microbiota function—acts as a rheostat that tunes pro-inflammatory activation of lymphocytes in the lamina propria. A major focus is placed on adherent-invasive Escherichia coli (AIEC), primarily associated with Crohn’s disease: beyond being identified and characterized, AIEC are portrayed as capable of driving mucosal CD4+ T cells toward pathogenic phenotypes through transdifferentiation. The most recent work discussed—conducted in collaboration with Milan-based research groups—further reports the identification of AIEC virulence factors responsible for Th17 cell transdifferentiation.

Taken together, these findings support the idea that targeted microbiota modulation could become a strategy to selectively reshape lymphocyte function, paving the way for precision medicine approaches in intestinal inflammation and beyond.