Combined effect of different lactic acid bacteria strains on the mode of cytokines pattern expression in human peripheral blood mononuclear cells.

The balance between immunogenic and tolerogenic activities in human immune system strongly depends on microflora-induced pro-and anti-inflamatory activities. Lactic acid bacteria (LAB) are important components of microflora. The interactions of the different strains of LAB and the cells of immune system are largely unknown. To assess if LAB strains composition would have an effect on the cellular responses profile (proliferation, cytokines synthesis) peripheral blood mononuclear cells (PBMC) model system was used. PBMC were induced by three different strains of LAB: Lactobacillus acidophilus, Lactobacillus delbrueckii spp. bulgaricus, Bifidobacterium bifidum. Tested strains were mixed together, in combinations with each other (pairs) or alone. Both, the LAB mixture as well as the pairs and the single LAB strains induced low lymphocyte proliferation (about 10% of ConA-induced response). However, the single LAB strains and their combinations were quite different cytokines inducers. First, L. acidophilus was much stronger IFN-y inducer than the LAB mixture, being a few times higher IL-12 stimulator than L. bulgaricus and B. bifidum. Second, L. bulgaricus and B. bifidum suppressed L.acidophilusinduced IFN-y synthesis to the level equal to that induced by the LAB mixture, limiting IL-12 production by about 30% and 70%, respectively. Third, the LAB strains were good IL-10 and TNF-alfa inducers, irrespectively of their combinations used. We conclude that LAB strains' pro or anti-inflammatory potentials are at least in part dependent on their composition. Low LAB mixture-induced IL-12 and IFN-y production and relatively high IL-10 and TNF-alfa expression may represent cellular activities normally induced in vivo by a combined action of bacterial antigens. Their presence is important to limit pro-inflammatory reactions (via IL-10) and to provide protection against infections (via TNF-alfa).