Heat-Killed Levilactobacillus brevis as a Candidate Postbiotics Through Immunostimulation Mediated by Macrophage-Inducible C-Type Lectin.

To understand the beneficial health-promoting effects of lactic acid bacteria (LAB) on immune cells, it is necessary to understand the relationship between LAB and innate immune receptors. We investigated the possible involvement of C-type lectin receptors (CLRs) in the immune-stimulating function of LAB in several strains. We found that levels of interleukin (IL)-6, tumor necrosis factor (TNF)-α, and IL-10 were reduced by the addition of inhibitors for spleen tyrosine kinase (syk), a signaling molecule used by several CLRs. Furthermore, employing CLR-Fc fusion proteins and reporter cells, we found that macrophage-inducible C-type lectin (Mincle) binds to Levilactobacillus brevis strain La37. Interestingly, this interaction was only observed in heat-killed L. brevis and disappeared after proteinase K treatment. Seven strains of L. brevis from different sources were also examined; among them, six strains showed Mincle reactivity, and the characteristics of the ligand were similar to those of La37. These results may facilitate a better understanding of the immunomodulatory effects of LAB for the development of functional foods.