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Objective: The objective of this study was to identify the immunomodulatory potential of two consortia of lactic acid bacteria,“Lab4” and “Lab4b”, using human macrophages as an in vitro model system.

Methods: THP-1 monocyte-derived macrophages were exposed to metabolites of Lab4 or Lab4b. RT-qPCR was performed on macrophages to determine the expression of M1 pro-inflammatory (IL-1β, IL-18 and CD80) or M2 antiinflammatory (CD206) marker mRNA in addition to IL-1β protein and inflammasome (NLRP3, Caspase-1, NLRP1, NLRC4 and AIM2) mRNA expression. Bacterial (LPS and ATP) and viral (Poly I: C) challenge were simulated to determine the potential of these consortia to regulate IL-1β protein, inflammasome mRNA expression, and antiviral IL-12 mRNA expression and protein under inflammatory conditions. The ability of these consortia to modulate macrophage phagocytosis of E. coli was also assessed.

Results: Lab4 and Lab4b metabolites promoted an M1 phenotype in macrophages in vitro by increasing mRNA expression of IL-1β, IL-18, and CD80 and reducing mRNA expression of CD206. Induction of IL-1β protein suggested involvement of the inflammasome. mRNA expression of NLRP3, Caspase-1, NLRP1 and AIM2 was induced by Lab4 and mRNA expression of NLRP3 and Caspase-1 was induced by Lab4b suggesting different potential modes of action of the two consortia. Lab4 and Lab4b metabolites, in combination with this LPS and ATP challenge, enhanced IL-1β mRNA and protein expression further, accompanied by different mRNA expression profiles of inflammasome genes by the two consortia. Lab4 and …