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* = Presenting author

P008 Common and different inflammatory features in inflammatory bowel disease and colon cancer

Lo Presti E.*1, Di Mitri R.2, Dieli F.1, Mocciaro F.2, Cilluffo M.G.3, Pecoraro G.M.4, Russo G.2, Meraviglia S.1

1University of Palermo, Department of Biopathology and Medical Biotechnologies (DIBIMED), University of Palermo; (CLADIBIOR), Palermo, Italy 2ARNAS Civico-Di Cristina-Benfratelli Hospital, Gastroenterology and Endoscopy Unit, Palermo, Italy 3A.O.U. Policlinico “G. Giaccone”, Gastroenterology and Hepatology Unit, Palermo, Italy 4Cattinara Hospital, Department of Gastroenterolgy, Trieste, Italy


The etiology of Inflammatory Bowel Disease (IBD) is complex and still, for the most part, obscure. Although the adaptive immune response has classically been considered to play a major role in the pathogenesis, there are evidence for involvement of tissue resident cells such as ILC, T gamma-delta and MAIT cells. The inflammatory response also plays an important role in CRC development. Since inflammation-associated tumorigenesis can rely on the interaction of pathogens and inflammatory cells, triggering the release of inflammatory cytokines and recruitment of other pro inflammatory cells, in this study we wanted to understand how in IBD treated patients, innate immune response can drive toward tumor evolution.


The identification of tissue resident immune cells was performed by flow cytometry after isolation and digestion of fresh intestinal biopsies, evaluating the frequency and the effector functions of ILC1, ILC3, MAIT and gamma-delta T cells. We analyzed a total of 52 samples: IBD at onset (n=12), IBD after therapy with Infliximab and Adalinumab (n=13), CRC (n=21), and healthy donors (n=6).


IFN gamma-producing ILC1 accumulated in IBD patients at onset, after treatment and in CRC. As expected TNF alpha-producing ILC1 were more abundant in IBD at onset and CRC. ILC3 producing IL17 but not IL22 accumulated in treated IBD patients and CRC but not in IBD at onset. Gamma-delta T cells with a predominantly effector phenotype were increased in IBD and in CRC. In particular, in CRC patients both gamma-delta T cells subsets were present, while in IBD patients the Vdelta1 subpopulation was more represented at onset but the Vdelta2 subset in treated patients. IL17 producing Vdelta1 cells accumulated in CRC but not in both IBD groups. Finally, MAIT cells were more represented in both groups of IBD than in CRC.


Our results, albeit preliminary, suggest that the innate immune system participates to gut inflammation and colorectal cancer, suggesting the intriguing possibility that certain inflammatory responses can be common to both pathologies and contribute to the development of chronic inflammation associated cancer.