{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T14:03:18Z","timestamp":1790172198806,"version":"4.1.0"},"reference-count":41,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T00:00:00Z","timestamp":1782864000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Food Science &amp; Nutrition"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    3\u2032\u2010sialyllactose (3\u2032\u2010SL) has demonstrated potential in regulating glycolipid metabolism and improving intestinal immunity, thereby exhibiting anti\u2010atherosclerotic (AS) properties. However, the mechanism by which 3\u2032\u2010SL exerts its anti\u2010AS effects through the regulation of inflammatory signaling via intestinal immunity remains unknown. Herein, 40 male low\u2010density lipoprotein receptor knockout (\n                    <jats:italic>LDLR<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    ) mice were randomized into five groups: normal diet (ND), high\u2010cholesterol diet (HCD), and three 3\u2032\u2010SL groups (low dose SLL, medium dose SLM, high dose SLH). After 12\u2009weeks, atherosclerotic plaque formation, serum lipids including total cholesterol (TC), triglycerides (TG), low\u2010density lipoprotein (LDL), high\u2010density lipoprotein (HDL), and inflammatory cytokines including interleukin\u20106 (IL\u20106), interleukin\u20101\u03b2 (IL\u20101\u03b2), interleukin\u201010 (IL\u201010) were measured. Multi\u2010omics analyses (gut microbiota 16S sequencing, colonic transcriptomics, and metabolomics) were performed. Compared with the HCD group, 3\u2032\u2010SL L intervention dose\u2010dependently and significantly reduced aortic lipid deposition in\n                    <jats:italic>LDLR<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice, lowered serum TG and LDL levels, increased HDL, while markedly decreasing pro\u2010inflammatory cytokines IL\u20106 and IL\u20101\u03b2 and elevating the anti\u2010inflammatory cytokine IL\u201010. Using the SLM group as representative for mechanistic exploration, it was found that 3\u2032\u2010SL reshaped the gut microbiota structure, significantly increasing the abundance of beneficial\n                    <jats:italic>Akkermansia<\/jats:italic>\n                    and reducing the\n                    <jats:italic>Firmicutes\/Bacteroidetes<\/jats:italic>\n                    ratio, thereby restoring microbial balance. Integrated multi\u2010omics analysis further revealed that 3\u2032\u2010SL drove colonic transcriptomic\u2010metabolic reprogramming, with enriched key pathways mainly involving immune regulation (e.g.,\n                    <jats:italic>Ccl2, Il2ra<\/jats:italic>\n                    ) and lipid metabolism (e.g.,\n                    <jats:italic>Kng1, C6<\/jats:italic>\n                    ). Differential metabolites showed significant correlations with immune\u2010 and cardiovascular\u2010related genes. Among these,\n                    <jats:italic>Ccl2<\/jats:italic>\n                    (MCP\u20101), as a key molecule linking gut immune signals to coronary artery pathology, was suppressed in expression, which may directly reduce the recruitment of monocytes\/macrophages into the subendothelial space, thereby inhibiting the initiation of atherosclerosis. Collectively, 3\u2032\u2010SL exhibits significant preventive effects against chronic inflammation in\n                    <jats:italic>LDLR<\/jats:italic>\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice with HCD\u2010induced atherosclerosis. These effects are mediated through synergistic regulation of metabolic, inflammatory, and microbial pathways along the gut microbiota\u2010immune\u2010cardiovascular axis. This axis integrates gut microbial metabolism, immune responses, and transcriptional signaling changes, revealing novel targets for the prebiotic 3\u2032\u2010SL in preventing atherosclerosis. It provides robust preclinical evidence for nutritional intervention strategies targeting the gut microbiota.\n                  <\/jats:p>","DOI":"10.1002\/fsn3.72053","type":"journal-article","created":{"date-parts":[[2026,7,1]],"date-time":"2026-07-01T15:55:11Z","timestamp":1782921311000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["3\u2032\u2010Sialyllactose Prevents Atherosclerosis by Attenuating Chronic Inflammation via the Gut\u2010Immune\u2010Cardiovascular Axis in\n                    <i>LDLR<\/i>\n                    <sup>\u2212\/\u2212<\/sup>\n                    Mice"],"prefix":"10.1002","volume":"14","author":[{"given":"Yingying","family":"Zhuang","sequence":"first","affiliation":[{"name":"Department of Clinical Nutrition, Zhongshan Hospital (Xiamen) Fudan University  Xiamen China"},{"name":"Xiamen Clinical Research Center for Cancer Therapy  Xiamen China"},{"name":"Xiamen Key Laboratory of Biotherapy  Xiamen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wei","family":"Zhang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Vaccines for Infectious Diseases, Xiang An Biomedicine Laboratory, National Innovation Platform for Industry\u2010Education Integration in Vaccine Research, School of Public Health, Xiamen University  Xiamen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Linlin","family":"Zhou","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Vaccines for Infectious Diseases, Xiang An Biomedicine Laboratory, National Innovation Platform for Industry\u2010Education Integration in Vaccine Research, School of Public Health, Xiamen University  Xiamen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hui","family":"Shu","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Vaccines for Infectious Diseases, Xiang An Biomedicine Laboratory, National Innovation Platform for Industry\u2010Education Integration in Vaccine Research, School of Public Health, Xiamen University  Xiamen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Wenqing","family":"Bo","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Vaccines for Infectious Diseases, Xiang An Biomedicine Laboratory, National Innovation Platform for Industry\u2010Education Integration in Vaccine Research, School of Public Health, Xiamen University  Xiamen China"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yiding","family":"Wang","sequence":"additional","affiliation":[{"name":"State Key Laboratory of Vaccines for Infectious Diseases, Xiang An Biomedicine Laboratory, National Innovation Platform for Industry\u2010Education Integration in Vaccine Research, School of Public Health, Xiamen University  Xiamen 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