Frontiers in nutrition · 2026
Multi-omics elucidation of Lactiplantibacillus plantarum NKK20 in preventing PCOS via the gut-ovary axis: SCFAs-mediated microbiota-metabolite-immune crosstalk.
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Xu Hao, Liu Xinyu, Sun Wen, Dong Xueyun, Liu Xuehui, Xie Yunhan, He Jiayuan, Ali Asmaa, Chen Min, Wu Liang, Ma Jie, Shao Keke
Аннотация
PURPOSE: Polycystic ovary syndrome (PCOS) is a clinically prevalent endocrine and metabolic disorder characterized by gut microbial disturbances and chronic low-grade inflammatory responses.
METHODS: This study explores the therapeutic potential and mechanistic insights of Lactiplantibacillus plantarum NKK20 (LP) in a PCOS murine model established through high-fat diet (HFD) and letrozole co-induction. By integrating multi-omics profiling (16S rRNA sequencing and untargeted metabolomics) with histopathological evaluation, we systematically assessed LP-mediated modulations of gut microbiota composition, metabolic signatures, ovarian function, and intestinal barrier integrity.
RESULTS: The results demonstrated that LP administration effectively counteracted metabolic dysregulation in PCOS mice, mitigating body weight gain, ameliorating lipid abnormalities (reduced total cholesterol, triglycerides, and LDL-C alongside elevated HDL-C), and lowering fasting glucose levels. Hormonally, LP suppressed hyperandrogenism, as evidenced by decreased testosterone, while rebalancing inflammatory mediators through IL-10 upregulation and concomitant reduction of TNF-α, IL-6, IL-1β, and MCP-1. Ovarian histomorphology revealed attenuated follicular cysts and enhanced luteinization. Critically, LP restored intestinal homeostasis by (i) augmenting short-chain fatty acid (SCFA) production-particularly butyrate-(ii) fortifying the gut barrier via increased ZO-1 and occludin expression, and (iii) diminishing circulating endotoxin. Microbial sequencing identified enrichment of Bacteroidetes and Muribaculum following LP treatment. Serum metabolomics further uncovered LP-induced normalization of steroid hormone biosynthesis and glycerophospholipid metabolism, coinciding with elevated anti-inflammatory mediators such as 6a-prostaglandin I1.
CONCLUSION: Collectively, these findings delineate a novel preventive axis through which LP inhibits PCOS progression - namely, via coordinated "gut microbiota-metabolite-ovarian" crosstalk involving SCFA-mediated barrier restoration, microbial ecology stabilization, and suppression of ovarian inflammatory onset. This work advances the translational rationale for probiotic-based strategies in PCOS prevention.
METHODS: This study explores the therapeutic potential and mechanistic insights of Lactiplantibacillus plantarum NKK20 (LP) in a PCOS murine model established through high-fat diet (HFD) and letrozole co-induction. By integrating multi-omics profiling (16S rRNA sequencing and untargeted metabolomics) with histopathological evaluation, we systematically assessed LP-mediated modulations of gut microbiota composition, metabolic signatures, ovarian function, and intestinal barrier integrity.
RESULTS: The results demonstrated that LP administration effectively counteracted metabolic dysregulation in PCOS mice, mitigating body weight gain, ameliorating lipid abnormalities (reduced total cholesterol, triglycerides, and LDL-C alongside elevated HDL-C), and lowering fasting glucose levels. Hormonally, LP suppressed hyperandrogenism, as evidenced by decreased testosterone, while rebalancing inflammatory mediators through IL-10 upregulation and concomitant reduction of TNF-α, IL-6, IL-1β, and MCP-1. Ovarian histomorphology revealed attenuated follicular cysts and enhanced luteinization. Critically, LP restored intestinal homeostasis by (i) augmenting short-chain fatty acid (SCFA) production-particularly butyrate-(ii) fortifying the gut barrier via increased ZO-1 and occludin expression, and (iii) diminishing circulating endotoxin. Microbial sequencing identified enrichment of Bacteroidetes and Muribaculum following LP treatment. Serum metabolomics further uncovered LP-induced normalization of steroid hormone biosynthesis and glycerophospholipid metabolism, coinciding with elevated anti-inflammatory mediators such as 6a-prostaglandin I1.
CONCLUSION: Collectively, these findings delineate a novel preventive axis through which LP inhibits PCOS progression - namely, via coordinated "gut microbiota-metabolite-ovarian" crosstalk involving SCFA-mediated barrier restoration, microbial ecology stabilization, and suppression of ovarian inflammatory onset. This work advances the translational rationale for probiotic-based strategies in PCOS prevention.