Lactic acid bacteria (LAB) are abundant in the gastrointestinal tract where they continuously regulate the immune system. NK cells are potently activated by dendritic cells (DCs) matured by inflammatory stimuli, and NK cells are present in the gut epithelium and in mesenteric lymph nodes, but it is not known how NK–DC interactions are affected by the predominantly non-pathogenic LAB. We demonstrate that human DCs exposed to different strains of gut-derived LAB consistently induce proliferation, cytotoxicity and activation markers in autologous NK cells. On the contrary, strains of LAB differ greatly in their ability to induce DC-dependent IFN-g production by NK cells. This suggests that DCs stimulated by gut LAB may expand the pool of NK cells and increase their cytotoxic potential. Specific LAB, inducing high levels of IL-12 in DCs, may promote amplification of a type-1 response via potent stimulation of IFN-g production in NK cells. Combining IFN-g-inducing and noninducing LAB completely abrogates DC-mediated IFN-g production by NK cells, and therefore LAB modulating IFN-g production in NK cells may be important regulators of the immune response.

Distinct gut-derived lactic acid bacteria elicitdivergent dendritic cell-mediated NK cell responses

FERLAZZO, Guido
2007-01-01

Abstract

Lactic acid bacteria (LAB) are abundant in the gastrointestinal tract where they continuously regulate the immune system. NK cells are potently activated by dendritic cells (DCs) matured by inflammatory stimuli, and NK cells are present in the gut epithelium and in mesenteric lymph nodes, but it is not known how NK–DC interactions are affected by the predominantly non-pathogenic LAB. We demonstrate that human DCs exposed to different strains of gut-derived LAB consistently induce proliferation, cytotoxicity and activation markers in autologous NK cells. On the contrary, strains of LAB differ greatly in their ability to induce DC-dependent IFN-g production by NK cells. This suggests that DCs stimulated by gut LAB may expand the pool of NK cells and increase their cytotoxic potential. Specific LAB, inducing high levels of IL-12 in DCs, may promote amplification of a type-1 response via potent stimulation of IFN-g production in NK cells. Combining IFN-g-inducing and noninducing LAB completely abrogates DC-mediated IFN-g production by NK cells, and therefore LAB modulating IFN-g production in NK cells may be important regulators of the immune response.
2007
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/11570/1670748
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