“…This process prevents the immune system from activating a proinflammatory response against commensal bacteria, while still maintaining the ability to protect against pathogens. When intestinal inflammation occurs, the mucosal barrier is interrupted and the specific epithelial receptors are expressed abnormally; a consequence of this is a greater intestinal permeability and susceptibility to the pathogenesis of AIEC (Antoni, Nuding, Wehkamp, & Stange, 2014;Benjamin, Makharia, Ahuja, Kalaivani, & Joshi, 2008;Sasaki et al, 2007;Smith, Thompson, O'Driscoll, & Clarke, 2013;Wine, Ossa, Gray-Owen, & Sherman, 2010). In the first moments of interaction, the ability of adhesion and invasion is given by flagella, Type 1 fimbria, outer membrane proteins (OmpCs) and…”