Background: Photoaging, induced by chronic ultraviolet B (UVB) exposure, results in the degradation of extracellular matrix (ECM) components, leading to skin roughness, wrinkle formation, and reduced elasticity. Recent studies have explored probiotics as potential inhibitors of extrinsic aging, primarily through mechanisms that protect the skin barrier and reduce collagen breakdown. Methods: This study investigates the anti-photoaging effects of Limosilactobacillus fermentum MG5368 (L. fermentum MG5368) and Lactiplantibacillus plantarum MG989 (L. plantarum MG989) in UVB-exposed keratinocytes and an SKH-1 hairless mice model. Results: Both strains demonstrated significant efficacy in preserving collagen through the inhibition of activating protein-1 (AP-1) and reducing the expression of matrix metalloproteinase (MMP)-1 and MMP-3. Additionally, both strains restored COL1A1 protein expressions, thereby enhancing collagen synthesis and ECM stability. Enhanced skin elasticity was observed, attributed to restored levels of hyaluronic acid and hyaluronan synthase 2 (HAS2) protein expressions. Conclusions: These findings suggest that L. fermentum MG5368 and L. plantarum MG989 may serve as promising probiotic-based agents for anti-photoaging applications.

Oral diseases such as periodontitis and dental caries, as well as conditions related to oral health such as halitosis, are closely associated with dysbiosis of the oral microbiota and continue to pose significant public health challenges worldwide. With the increasing resistance to existing antibiotics and side effects of chemical disinfectants, probiotics have emerged as promising alternatives for oral healthcare. This study aimed to evaluate the oral health efficacy and probiotic properties of Limosilactobacillus fermentum (L. fermentum) MG4717 isolated from the human oral cavity. L. fermentum MG4717 showed notable antimicrobial activity against the key oral pathogens Streptococcus mutans (S. mutans), Aggregatibacter actinomycetemcomitans (A. actinomycetemcomitans), Porphyromonas gingivalis (P. gingivalis), and Fusobacterium nucleatum (F. nucleatum) and effectively inhibited biofilm formation. Additionally, L. fermentum MG4717 significantly downregulated methionine gamma-lyase (mgl) mRNA expression in P. gingivalis, which is implicated in halitosis and pathogenicity. L. fermentum MG4717 strongly adhered to the KB and HT-29 epithelial cells and exhibited good resilience under simulated gastrointestinal conditions. Whole-genome sequencing (WGS) and average nucleotide identity (ANI) analysis confirmed strain identity (98.73% average nucleotide identity with L. fermentum DSM20052) and the absence of transferable antibiotic resistance genes. Safety assessments revealed no cytotoxicity, hemolytic activity, or bile salt hydrolase activity. These findings suggest that L. fermentum MG4717 has the potential to be used as a safe and effective oral probiotic beneficial for oral health.

Probiotics have recently gained attention as modulators of the gut–brain axis in neurodegenerative diseases such as Alzheimer’s disease. In this study, we identified probiotic strains with neuroprotective effects and investigated their mechanisms and safety. We screened strains based on their ability to inhibit acetylcholinesterase (AChE) activity and protect cells against H₂O₂-induced damage. The cell-free supernatants (CFS) of Lactobacillus gasseri MG4247 and Lacticaseibacillus rhamnosus MG4644 inhibited AChE activity and reduced cell damage and reactive oxygen species generation. These effects were mediated through inhibition of the MyD88/NF-κB pathway and modulation of the JNK/Bax-dependent apoptotic pathway in neuronal cells treated with H₂O₂. Whole-genome sequencing and antibiotic susceptibility testing confirmed the identity and safety of both strains. These findings suggest that MG4247 and MG4644, as probiotics, may help protect neuronal cells from oxidative stress and inflammation.

Background/Objectives: Glucagon-like peptide-1 receptor agonists (GLP-1RAs) are effective treatments for obesity, but substantial weight regain is common after therapy is discontinued. This study investigated whether probiotic strains with anti-obesity effects could enhance GLP-1RA-induced weight loss and attenuate post-treatment weight rebound. Methods: Candidate lactic acid bacteria were screened for anti-obesity efficacy in a high-fat-diet (HFD)-induced obese mouse model, and the selected strain was further characterized using metabolomic profiling of culture supernatants. To examine its interaction with GLP-1RA therapy, obese mice received dulaglutide for 4 weeks and were monitored for 2 weeks after treatment withdrawal, while the probiotic was orally administered for a total of 6 weeks. Body weight, glycemic parameters, and muscle strength were assessed throughout the study. Results: Limosilactobacillus fermentum GB102 reduced body weight and improved glycemic control in HFD-fed mice. These metabolic benefits were associated with alterations in circulating metabolic hormones, including adipokines, along with attenuated inflammatory responses in adipose tissue. Metabolomic profiling revealed that GB102 produced high levels of succinic acid, a metabolite previously linked to thermogenic activation. This strain increased whole-body energy expenditure in HFD-fed mice, produced glutamine, and showed enhanced conversion of arginine into ornithine and citrulline. When combined with dulaglutide, GB102 enhanced weight loss, preserved muscle strength, and attenuated both weight regain and glycemic rebound following dulaglutide withdrawal. Conclusions: These findings suggest that energy-metabolism-enhancing probiotics such as GB102 may enhance the metabolic effects of GLP-1RA therapy and help attenuate weight regain after treatment discontinuation.

Background/Objectives: This study investigated the systemic metabolic effects of two probiotic strains, Lacticaseibacillus paracasei MG5012 and Bifidobacterium animalis subsp. lactis MG741, on metabolic dysfunction-associated steatotic liver disease (MASLD) and obesity-related muscle dysfunction in high-fat-diet (HFD)-induced obese mice. Methods: Obesity was induced in C57BL/6 mice via high-fat diet (HFD) feeding for 6 weeks. Subsequently, the mice were orally administered MG5012 or MG741 for 8 weeks. We assessed systemic metabolic parameters, including body weight, adiposity, and serum biomarkers. Additionally, histological and molecular analyses were performed to evaluate hepatic steatosis, intestinal barrier integrity, and muscle oxidative status. Results: Both strains significantly attenuated body weight gain and adiposity, reduced serum liver injury markers (γ-GTP, ALT, AST), and improved systemic metabolic parameters by restoring serum GLP-1 levels and reducing hyperinsulinemia. Crucially, MG5012 and MG741 strengthened intestinal barrier integrity by upregulating the tight junction proteins Occludin and Claudin-1. In the liver, histological analyses revealed reductions in hepatic steatosis and triglyceride content, accompanied by the downregulation of lipogenic genes (SREBP-1c, FAS). Furthermore, the probiotics preserved skeletal muscle integrity; while muscle weight remained unchanged, the strains increased muscle fiber cross-sectional area (CSA) and reduced serum markers of muscle damage (CPK, LDH). This protective effect was associated with significantly enhanced expression of antioxidant enzymes (SOD, CAT, GPx) in muscle tissue. Conclusions: These findings suggest that MG5012 and MG741 confer systemic metabolic benefits through the modulation of the gut–liver–muscle axis and may serve as promising functional food ingredients for the management of MASLD and obesity-associated muscle atrophy.

In this study, we investigated the effects of MG4244 on intestinal permeability, oxidative stress, and lipid accumulation in Caenorhabditis elegans with metabolic inflammation induced by Pseudomonas aeruginosa (PA) and a high-glucose diet (HGD). The worms infected with PA exhibited increased intestinal permeability and reactive oxygen species (ROS) production, which were improved upon MG4244 treatment. Also, MG4244 inhibited lipid and ROS accumulation induced by an HGD. In addition, MG4244-treated worms showed extended lifespans under various conditions. To elucidate the mechanism of the MG4244 effects, we conducted further investigation using mutant strains with knockdown of genes associated with the AMP-activated protein kinase (AMPK) and mitogen-activated protein kinase (MAPK) pathways. The results demonstrated that the MG4244 effect on lipid metabolism was primarily mediated through the AMPK signaling pathway. Furthermore, MG4244 enhanced pathogen resistance by MAPK signaling pathways, mitigating stress responses, and maintaining intestinal integrity. In further studies, combined treatment with PA and an HGD significantly increased intestinal permeability, lipid, and ROS levels, confirming their negative synergistic effects. However, MG4244 under PA and HGD co-treatment conditions effectively mitigated these health disruptions, suggesting a protective role of MG4244. This study provides an in vivo platform using C. elegans to evaluate probiotic efficacy related to the intestinal environment. Also, our results highlight the therapeutic potential of MG4244 in improving resilience to metabolic inflammation through gut-targeted mechanisms.