Lactobacillus paracasei KW3110 (KW3110) has anti-inflammatory effects, including the prevention of blue light exposure induced
retinal inflammation and ageing-related chronic
inflammation in mice. The mechanism involves the promotion of anti-inflammatory
cytokine interleukin (IL)-10 production by KW3110, leading to reduced pro-inflammatory
cytokine IL-1β production. Although various stress-induced mitochondrial damages are associated with excessive inflammatory responses, the effect of KW3110 on inflammatory-stress-induced mitochondrial damage remains unknown. In this study, we investigated the effect of KW3110 on inflammatory stress-induced mitochondrial damage using the murine macrophage-like cell line J774A.1. KW3110 treatment suppressed
lipopolysaccharide (LPS)-induced
mitochondrial dysfunction, including downregulation of membrane potential, induction of
reactive oxygen species, and respiratory dysfunction. In addition, KW3110 prevented LPS-induced disruption of mitochondrial morphology including cristae structures.
IL-10 treatment also ameliorated LPS-induced
mitochondrial dysfunction and morphology disruption. These results suggest that KW3110 prevents LPS-induced
mitochondrial dysfunction, potentially via promoting
IL-10 production in mouse macrophages. We are the first to reveal a suppressive effect of lactic acid bacteria on mitochondrial morphology disruption in inflammatory-stressed macrophages. Our findings contribute to understanding inflammatory-stress-induced mitochondrial damage and developing
food ingredients with preventive effects on mitochondrial-damage-derived inflammatory conditions.