Selected commensal bacteria change profiles of Helicobacter pylori-induced T cells via dendritic cell modulation.

Abstract

The mechanisms of downregulation of protective immunity against Helicobacter pylori (Hp) infection strongly depend on dendritic cell (DC)-induced T-lymphocyte differentiation pattern. Lactic acid bacteria (LAB) strains can modulate Hp-induced immunoresponse by changes in DC activation profiles. Here, we want to find out if the LAB-pulsed DCs will change Hp-induced T-cell responsiveness patterns. The naive peripheral CD4+ T cells were co-cultured with Hp CagA+pulsed monocyte-derived DCs (DC/CD4+ T cell) in the presence/absence of the feces-derived probiotics: antagonistic or non-antagonistic to Hp (Lactobacillus rhamnosus 900, Lr, Lactobacillus paracasei 915, Lp, respectively), as assessed by the agar slab method. The regulatory T-cell (Treg) population was assessed by flow cytometry, and IFN-γ, IL-12p70, IL-10, and IL-17A levels were evaluated by ELISA method. The Hp-pulsed DC/CD4+ T-cell co-cultures were characterized by high IL-10, decreased IL-12p70 and IFN-γ levels, and elevated Treg population. In contrast, Lr-pulsed DC/CD4+ T-cell co-cultures expressed low IL-10, high IL-12p70 and IFN-γ levels and declined Treg population; this responsiveness pattern was not changed by Hp. The responsiveness pattern of the Lp/Hp-pulsed DC/CD4+ T-cell co-cultures did not differ from those pulsed with Hp alone. In contrast to Lp, Lr probiotic strain overcomes Hp-mediated immune profile in the DC/T-cell co-cultures toward Th1 pattern and limited generation of Tregs in vitro. Lr may therefore be used as a component of anti-Hp treatment.