CONICET | Buscador de Institutos y Recursos Humanos

Background. Crohn´s disease and ulcerative colitis are chronic inflammatory intestinal diseases, collectively referred as inflammatory bowel diseases (IBD). In spite of their high incidence, characterization of the molecular pathways involved in their onset and development is far from complete. With an interdisciplinary approach, we investigate how the transition from healthy to inflamed mucosa can modulate the glycome of immune cells and potentially mediate cellular processes relevant to immune tolerance and disease. In this study, we focus on characterizing the glycophenotype of B cells isolated from the gut and its response to local inflammation in experimental models of colitis.Methods. We purified lymphocytes from different gut-associated lymphoid tissues in C57BL6/J mice. To study potential modifications of the B cell glycome induced by inflammatory conditions, we used the 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis as a model. B cell glycophenotype was characterized using biotinylated lectins and flow cytometry.Results. B cells from the lamina propria showed a glycophenotype rich in complex N-glycans and alpha2,6 sialic acid, different to B cells isolated from appendix lymphoid tissue and Peyer´s Patches. Inflammatory conditions induce specific changes in the level of complex N-glycans in B cells from lamina propria, and in alpha2,6 sialylation in B cells from mesenteric lymph nodes.Conclusions. B cells from gut-associated lymphoid tissues exhibit a differential glycophenotype depending on anatomic location and can be modulated by inflammatory conditions. These differences could be relevant to the physiological function of B cells in different compartments, and could eventually play a role in the pathogenesis of IBD.