{
  "abstract": "Inflammatory bowel disease (IBD) involves dysregulated host immunity, gut microbial dysbiosis, and metabolic disturbances. As key innate immune cells, macrophages play critical roles in inflammatory responses, epithelial barrier dysfunction, and host-microbiota interactions. Tumor necrosis factor receptor-associated factor 6 (TRAF6) is a key adaptor protein in pro-inflammatory signaling, but the role of macrophage TRAF6 in colitis-associated microbial and metabolic alterations remains unclear. Here, we used macrophage-specific Traf6 conditional knockout mice in a 3% DSS-induced colitis model. TRAF6 expression was increased in colonic tissues from DSS-treated mice and patients with IBD, with enhanced co-localization with CD68-positive macrophages. Macrophage-specific Traf6 deletion reduced colitis severity, inflammatory responses, and epithelial barrier injury. 16S rRNA gene sequencing showed substantial gut microbiota remodeling, including reduced Enterococcus abundance. Untargeted metabolomics identified alterations in arachidonic acid metabolism: prostaglandin A2 (PGA2) was significantly reduced in both fecal and serum samples, whereas 12(S)-hydroxy-5Z,8E,10E-heptadecatrienoic acid [12(S)-HHT] was significantly reduced in feces and showed a similar downward trend in serum. Enterococcus abundance was positively associated with PGA2 and 12(S)-HHT levels, and an independent human IBD cohort further showed enrichment of Enterococcus. Collectively, macrophage-specific Traf6 deletion ameliorated DSS-induced colitis and was associated with coordinated remodeling of the gut microbiota and host metabolism, supporting an association between macrophage TRAF6, reduced Enterococcus abundance, and altered arachidonic acid metabolism during intestinal inflammation.",
  "abstract_shown": true,
  "affiliations": [
    "Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Key Laboratory of Fertility Preservation and Maintenance of Ministry of Education, Ningxia Medical University, Yinchuan, China.",
    "The First Clinical Medical School, Ningxia Medical University, Yinchuan, China.",
    "Department of Gastroenterology, General Hospital of Ningxia Medical University, Yinchuan, China. wangfang9803@163.com.",
    "Key lab of ministry of education for protection and utilization of special biological resources in western China, Ningxia University, Yinchuan, China. wuxiaol@nxu.edu.cn.",
    "Department of Biochemistry and Molecular Biology, School of Basic Medical Sciences, Key Laboratory of Fertility Preservation and Maintenance of Ministry of Education, Ningxia Medical University, Yinchuan, China. gaoyujing2004@126.com."
  ],
  "article_type": "research article",
  "arxiv": null,
  "author_total": 8,
  "authors": [
    {
      "affs": [
        0
      ],
      "name": "Qinmei Ma"
    },
    {
      "affs": [
        0
      ],
      "name": "Fang Li"
    },
    {
      "affs": [
        1
      ],
      "name": "Mingdi Wang"
    },
    {
      "affs": [
        1
      ],
      "name": "Xiuyi Fang"
    },
    {
      "affs": [
        1
      ],
      "name": "Jinhan Sun"
    },
    {
      "affs": [
        2
      ],
      "name": "Fang Wang"
    },
    {
      "affs": [
        3
      ],
      "name": "Xiaoling Wu"
    },
    {
      "affs": [
        4
      ],
      "name": "Yujing Gao",
      "orcid": "0000-0003-0718-4992"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/6ekvye1czd79d.bib",
  "cited_by": 0,
  "doi": "10.1186/s12866-026-05536-0",
  "fulltext_url": "https://europepmc.org/articles/PMC13753423",
  "id": "6ekvye1czd79d",
  "issns": [
    "1471-2180"
  ],
  "landing_url": "https://europepmc.org/article/MED/43009771",
  "language": "eng",
  "licence": "CC-BY-NC-ND",
  "licence_label": "CC BY-NC-ND",
  "licence_source": "article",
  "licence_url": "https://creativecommons.org/licenses/by-nc-nd/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "openalex",
      "2715|Inflammatory Bowel Disease"
    ]
  ],
  "openalex": "W7202362899",
  "pdf_url": "https://europepmc.org/articles/PMC13753423?pdf=render",
  "pmcid": "PMC13753423",
  "pmid": "43009771",
  "published": "2026-08-13",
  "publisher": null,
  "ris": "https://research.draconitic.com/paper/6ekvye1czd79d.ris",
  "sources": [
    {
      "first_seen": "2026-11-12T15:22:43Z",
      "native_id": "MED:43009771",
      "source": "europepmc",
      "url": "https://europepmc.org/article/MED/43009771"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "openalex:2715|Inflammatory Bowel Disease",
      "subfield": "general"
    }
  ],
  "title": "Macrophage-specific TRAF6 deletion mitigates DSS-induced colitis and is associated with reduced Enterococcus abundance and altered arachidonic acid metabolism.",
  "title_text": "Macrophage-specific TRAF6 deletion mitigates DSS-induced colitis and is associated with reduced Enterococcus abundance and altered arachidonic acid metabolism.",
  "type": "peer-reviewed",
  "updated_at": "2026-11-13T03:20:45Z",
  "url": "https://research.draconitic.com/paper/6ekvye1czd79d",
  "venue": "BMC microbiology",
  "versions": []
}