Authors: Fabio Turco, Paolo Andreozzi, Ilaria Palumbo, Francesco Paolo Zito, Martina Cargiolli, Walter Fiore, Nicola Gennarelli, Giovanni Domenico De Palma, Giovanni Sarnelli, Rosario Cuomo


  • Department of Clinical Medicine and Surgery, Federico II University of Naples, Naples, Italy
  • Sofar S.p.A. Trezzano Rosa, Italy

Publication: United European Gastroenterology Journal

Date: December 2016

Full paper:


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 pro-inflammatory effects exerted by EIEC, suggesting a beneficial role of this probiotic in DD.