Related Experiment Video
Updated: Oct 3, 2025
Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes
Published on: May 31, 2018
Lactobacillus paracasei KW3110 Prevents Inflammatory-Stress-Induced Mitochondrial Dysfunction in Mouse Macrophages
Takahiro Yamazaki1, Sayuri Yamada1, Konomi Ohshio1
1KIRIN Central Research Institute, Kirin Holdings Co., Ltd., Fujisawa 251-8555, Kanagawa, Japan.
Abstract:
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.
Insights
Lactobacillus paracasei KW3110 prevents inflammation-induced mitochondrial damage in macrophages by enhancing interleukin-10 production. This probiotic may offer protective effects against inflammatory conditions linked to mitochondrial dysfunction.
Area of Science:
- Immunology
- Microbiology
- Cell Biology
Background:
- Lactobacillus paracasei KW3110 exhibits anti-inflammatory properties.
- Inflammatory responses are often linked to mitochondrial damage.
- The effect of KW3110 on inflammatory-stress-induced mitochondrial damage was previously unknown.
Purpose of the Study:
- To investigate the impact of Lactobacillus paracasei KW3110 on inflammatory stress-induced mitochondrial damage.
- To elucidate the role of interleukin-10 in mediating these protective effects.
Main Methods:
- Murine macrophage-like cell line J774A.1 were treated with KW3110 and lipopolysaccharide (LPS).
- Mitochondrial function was assessed by measuring membrane potential, reactive oxygen species production, and respiratory function.
- Mitochondrial morphology, including cristae structures, was examined.
Main Results:
- KW3110 suppressed LPS-induced mitochondrial dysfunction, including reduced membrane potential, increased reactive oxygen species, and impaired respiration.
- KW3110 prevented LPS-induced disruption of mitochondrial morphology.
- Interleukin-10 treatment mimicked the protective effects of KW3110 on mitochondrial dysfunction and morphology.
Conclusions:
- Lactobacillus paracasei KW3110 protects macrophages against inflammatory stress-induced mitochondrial damage.
- These protective effects are potentially mediated by the promotion of interleukin-10 production.
- This study reveals a novel suppressive effect of lactic acid bacteria on mitochondrial morphology disruption in inflammatory-stressed macrophages.
