Bacterial stimuli activate nitric oxide colonic mucosal production in diverticular disease. Protective effects of L. casei DG® (Lactobacillus paracasei CNCM I-1572). Issue 5 (August 2017)

• Record Type: Journal Article
• Authors: Turco, Fabio; Andreozzi, Paolo; Palumbo, Ilaria; Zito, Francesco Paolo; Cargiolli, Martina; Fiore, Walter; Gennarelli, Nicola; De Palma, Giovanni Domenico; Sarnelli, Giovanni; Cuomo, Rosario
• Is Part Of: United European Gastroenterology journal. Volume 5:Issue 5(2017)
• Page Start: 715
• Page End: 724
• Publication Date: 2017-08
• Subjects: Diverticular disease -- probiotic -- nitric oxide -- human colonic mucosa -- enteroinvasive Escherichia coli; Gastroenterology -- Periodicals; Periodicals; 616.33005
• DOI: 10.1177/2050640616684398
• Languages: English
• ISSNs: 2050-6406

Abstract

Background: Micro-inflammation and changes in gut microbiota may play a role in the pathogenesis of diverticular disease (DD). Objective: 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. Methods: 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. Results: 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. Conclusions: Colonic mucosa of patients with DD is characterized by a different reactivity toward pathogenic stimuli. LCDG plays a role in counteracting the pro-inflammatory effects exerted by EIEC, suggesting a beneficial role of this probiotic in DD.