{"id":246,"title":"The gut-placental axis: microbial signals remodeling maternal-fetal immune tolerance","title_zh":"肠-胎盘轴：微生物信号如何重塑母胎免疫耐受","url":"https://pubmed.ncbi.nlm.nih.gov/42979195","doi":"10.3389/fimmu.2026.1971075","pmid":"42979195","journal":"Front Immunol","kind":"paper","lang":"en","published_at":"2026-10-20T00:00:00+00:00","fetched_at":"2026-11-08T03:44:00+00:00","authors":["Shi L","Li Y","Mo Y"],"primary_topic":"endometrium","topics":[{"slug":"endometrium","score":7.0,"hits":["maternal-fetal interface","placenta","placental","uterine"]},{"slug":"repro-immunology","score":7.0,"hits":["immune tolerance","macrophage","regulatory t cell","treg"]},{"slug":"early-pregnancy","score":4.0,"hits":["preeclampsia","pregnancy outcomes","preterm birth","recurrent pregnancy loss"]},{"slug":"ethics-policy","score":1.0,"hits":["regulatory"]}],"topic_score":7.0,"preference_score":0.0,"preference_labels":[],"llm_score":74.0,"final_score":74.0,"score_dims":{"novelty":72,"rigor":65,"impact":75,"relevance":78,"translation":62},"recommend_reason":"选题横跨生殖免疫与微生物组，系统整合了肠道信号调控母胎耐受的多条分子通路，并对“胎盘微生物组”争议给出清晰立场，适合作为机制梳理与课题设计的参考；但属叙述性综述、无原始数据，转化结论仍以假说为主，不宜作为临床决策依据。","keywords":["肠-胎盘轴","母胎免疫耐受","肠道菌群代谢物","调节性T细胞","妊娠并发症","细胞外囊泡"],"selected":1,"story_id":362,"llm_provider":"deepseek","llm_model":"deepseek-flash","llm_effort":"low","source_key":"pubmed-uterus-pregnancy","source_name":"PubMed · 内膜/植入/早孕","source_tier":1,"mention_count":1,"has_interpretation":false,"journal_key":"front-immunol","journal_tier":"standard","journal_if":5.7,"is_mock":false,"summary_zh":"本文为叙述性综述，提出“肠-胎盘免疫轴”概念，系统梳理肠道菌群信号经短链脂肪酸、色氨酸衍生物及AhR配体、次级胆汁酸、微生物相关分子模式、细菌胞外囊泡与胎盘外泌体等途径，远程调控母胎界面免疫细胞（MDSC、RORγt+ pTreg等Treg亚群、Th17/Treg平衡、巨噬细胞极化、子宫NK细胞）的分子机制。作者强调以“分子信号传递”而非活菌定植为主导范式，并讨论肠道菌群失调在子痫前期、妊娠期糖尿病、复发性流产、早产与胎儿生长受限中的病理级联，评估益生菌、膳食纤维、后生元及工程化囊泡的转化前景，同时区分人体关联证据与动物因果证据。","summary":"Pregnancy represents a unique immunological challenge requiring the establishment and maintenance of maternal-fetal immune tolerance. Emerging evidence demonstrates that the gut microbiota serves as a critical regulator of placental immune responses through systemic immune remodeling, constituting what is now recognized as the gut-placental immune axis. This narrative review examines the molecular pathways through which intestinal signals reach the maternal-fetal interface, encompassing short-chain fatty acids, tryptophan derivatives and their aryl hydrocarbon receptor (AhR) ligands, secondary bile acids, microbe-associated molecular patterns, bacterial extracellular vesicles, and placental exosomes. These signals collectively regulate key immune cell populations, including myeloid-derived suppressor cells, regulatory T cell subsets such as RORγt+ peripherally derived regulatory T cell (pTreg), Th17/Treg balance, macrophage polarization, and uterine natural killer (NK) cell function. We critically address the placental microbiome controversy, emphasizing that molecular signal transmission rather than live microbial colonization represents the prevailing paradigm for gut-placental communication. This paradigm shift redirects the research focus from identifying bacterial species to characterizing bioactive metabolites and microbe-associated molecular patterns. Furthermore, we elucidate how gut dysbiosis drives pathological cascades in major pregnancy complications, including preeclampsia, gestational diabetes mellitus, recurrent pregnancy loss, preterm birth, and fetal growth restriction. Finally, we evaluate clinical translation prospects encompassing probiotics, dietary fiber interventions, postbiotic metabolite supplementation, and engineered extracellular vesicle therapies, while acknowledging persistent challenges in establishing causal relationships, addressing individual heterogeneity, and ensuring long-term safety. This conceptual framework advances mechanistic understanding of microbiota-immune-placenta interactions and provides a foundation for developing microbiota-informed strategies to predict and prevent adverse pregnancy outcomes. Throughout, we explicitly distinguish human associative evidence from animal causal evidence.","interpretation_basis":null,"fulltext_status":null,"interpretation":null,"fulltext":{"available":false,"status":null,"reason":"尚未抓取全文（未入选、分数未达阈值，或还没跑 fulltext 步骤）","pmcid":null,"license":null,"chars":0,"source":null,"fetched_at":null}}