Another possibility is that both processes could be related to a coordinated expression, SB273005 datasheet for instance, by the EnvZ/OmpR regulatory system. Rohlion et al [38] recently proposed a model in which OmpC,

a porin regulated by EnvZ/OmpR, has been implicated in the adherence-invasiveness of AIEC, and this system is also known to play an important role in biofilm formation [39]. The biofilm formation could also be dependent on the cyclic di-GMP Selleck BKM120 concentration which was recently reported to regulate the expression of type 1 pili and flagella in AIEC reference strain LF82 [40]. Biofilms in the human gut are thought to play an agonistic role with the host [18], being necessary to achieve an homeostatic situation and appropriate gut physiology. Nevertheless, previous studies have highlighted the increased biofilm formation in patients with CD with respect to control subjects [41]. Moreover, the composition of the mucosa-associated microbiota is altered with respect to that of non-IBD controls [42]. It is widely accepted that the intestinal microbiota is essential to elicit the inflammation; however, the specific role of intestinal biofilms in CD is still uncertain. Changes in the composition and abundance of mucosa-associated biofilms have been proposed either to play LEE011 purchase a role in the onset or perpetuation of CD [41, 43–45] or to be a consequence of

the defective immune regulation in CD patients [18, 46, 47]. Because we have analyzed the biofilm formation capacity of a collection of AIEC and non-AIEC strains using an in vitro method we can deduce that the ability of AIEC to form biofilms is irrespective of host factors. However, in vivo experiments would give interesting insights into the pathogenesis of AIEC in CD. Biofilm formation of AIEC in human gut, if confirmed, Glutamate dehydrogenase would confer to the pathovar an advantage for colonization of the intestine. Consequently, given the

pathogenic behavior of AIEC, a more stable colonization would increase their probability of invading the intestinal epithelium and further trigger mucosal inflammation and, possibly, granuloma formation. In this sense, and speculatively, biofilm formation could contribute to AIEC pathogenesis. Conclusion A novel phenotypic trait of AIEC pathovar was described in this work. Biofilm production ability of AIEC strains could be an additional trait involved in their pathogenesis. Further investigations to detect AIEC specific genetic determinants involved in biofilm formation and to analyze the genetic regulatory processes are essential to fully understand AIEC pathogenesis and elucidate a possible role of AIEC in CD. Methods Bacterial strains Amongst the collection of 65 E. coli strains, sixty-one (93.8%) were isolated from human intestinal mucosa in previous studies [15, 48].