Micro-inﬂammation and changes in gut microbiota may play a role in the pathogenesis of diverticular disease (DD).
The objective of this article is to evaluate the expression of nitric oxide (NO)related mediators and S100B in colonic mucosa of patients with DD in an ex vivo model of bacterial infection.
Intestinal biopsies obtained from patients with diverticulosis, symptomatic uncomplicated diverticular disease (SUDD) and SUDD with previous acute diverticulitis (SUDD+AD) were stimulated with the probiotic L. casei DG® (LCDG) and/or the pathogen enteroinvasive Escherichia coli (EIEC). S100B, NO release and iNOS expression were then evaluated.
Basal iNOS expression was signiﬁcantly increased in SUDD and SUDD+AD patients. Basal NO expression was signiﬁcantly increased in SUDD+AD. No diﬀerences in S100B release were found. In all groups, iNOS expression was signiﬁcantly increased by EIEC and reduced by LCDG. In all groups, except for SUDD+AD, EIEC signiﬁcantly increased NO release, whereas no increase was observed when LCDG was added to biopsies. EIEC did not induce signiﬁcant changes in S100B release.
Colonic mucosa of patients with DD is characterized by a diﬀerent reactivity toward pathogenic stimuli. LCDG plays a role in counteracting the proinﬂammatory eﬀects exerted by EIEC, suggesting a beneﬁcial role of this probiotic in DD
Turco F, Andreozzi P, Palumbo I, Zito FP, Cargiolli M, Fiore W, Gennarelli N, De Palma GD, Sarnelli G, Cuomo R.
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