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The gastrointestinal tract is one of the most colonized organs and harbors a large microbial population (1014 bacteria) that has co-evolved with us establishing a finely tuned symbiosis (Ley et al., 2008). As a result of their occurrence in complex mixtures, their combined genomes or metagenome, contain 150-fold more genes respect to humans, therefore providing us with novel functions (Qin et al., 2010). Increasing evidences show that the disruption of this symbiosis may lead to pathologies such as obesity or to an increased risk of developing inflammatory bowel disease (Ott et al., 2004). Since the intestine is constantly exposed to an almost limitless number of foreign antigens (i.e., food-derived materials, commensal microbes, pathogenic bacteria, viruses and parasites), it is of fundamental importance that an appropriate immune homeostasis in the gut mucosa is established and maintained. This requires a highly sophisticated immunological regulatory systems achieved by the cooperative interaction of intestinal epithelial cells (IECs) and mucosal cells of the immune response (Goto and Kiyono, 2011). The IECs comprise columnar epithelial cells, Paneth cells, endocrine cells and goblet cells (van der Flier and Clevers, 2009) and consist in the first physical barrier between the host and the external environment. Owing to many signals transmission from epithelial cells to the various innate and acquired types of mucosal cells of the immune response, these cells regulate each other resulting in intestinal immunological homeostasis.

Interplays between gut microbiota and gene expression regulation by miRNAs