ORIGINAL RESEARCH article
Front. Microbiol.
Sec. Food Microbiology
This article is part of the Research TopicProbiotic Potential: Lactic Acid Bacteria in Advancing Functional Foods and Health OutcomesView all 4 articles
Lactobacillus gasseri CBT LGA2 Alleviates Muscle Protein Degradation and Inflammation in Immobilization-induced Mouse
Provisionally accepted
- 1Korea University - Sejong Campus, Sejong, Republic of Korea
- 2Cell Biotech International Co Ltd, Gyeonggi-do, Republic of Korea
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This study investigated the protective effects of Lactobacillus gasseri CBT LGA2 (LGA2) against disuse-induced muscle atrophy and inflammation using both in vitro and in vivo models. Among five probiotic strains screened, LGA2 most effectively suppressed dexamethasone-induced muscle protein degradation in C2C12 myotubes and lipopolysaccharide-induced inflammatory responses in RAW264.7 macrophages. Whole-genome analysis confirmed its genetic safety and revealed functional genes related to antioxidant defense, immune modulation, and muscle protection. In a hindlimb immobilization mouse model, oral administration of LGA2 (1 × 10⁸ CFU/kg/day for three weeks) significantly alleviated muscle atrophy, improving grip strength, preserving muscle mass, and restoring muscle fiber cross-sectional area. LGA2 maintained phosphorylation of FOXO3a, suppressed muscle-specific E3 ubiquitin ligases (Atrogin-1, MuRF1), and reversed the downregulation of myogenin and MyHC isoforms (IIa, IIx, IIb). These changes indicate reduced proteolysis and recovery of myogenic potential. Moreover, LGA2 decreased pro-inflammatory cytokines (TNF-α, IL-6, iNOS, COX-2) and restored anti-inflammatory IL-10 levels in muscle and serum. Collectively, these findings demonstrate that LGA2 prevents disuse-induced muscle atrophy through coordinated anti-inflammatory, anti-proteolytic, and pro-myogenic mechanisms, supporting its potential as a safe and functional probiotic intervention.
Keywords: Lactobacillus gasseri, Probiotics, muscle atrophy, Inflammation, hindlimb immobilization, Sarcopenia
Received: 19 Oct 2025; Accepted: 27 Nov 2025.
Copyright: © 2025 Hun Jang, Lim, Choi, Lim and Oh. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
* Correspondence: Namsu Oh
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