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<p>Aflatoxin B1 (AFB1) is a prevalent mycotoxin in poultry feed, yet its impact on avian influenza virus H3N8 infection remains poorly understood. Here, we show that environmentally relevant concentrations of AFB1 (25–100 μg/kg) significantly enhance H3N8 replication both in chicken cell lines (DF-1 and CEF) and in specific pathogen-free (SPF) chickens. Using a multi-omics approach integrating histopathology, 16S rRNA sequencing, and untargeted metabolomics, we demonstrate that AFB1 exposure disrupts intestinal barrier integrity, induces gut dysbiosis, and specifically reduces the colonization of beneficial segmented filamentous bacteria (SFB) on the ileal epithelium. This was associated with altered lipid metabolism, notably increased levels of dodecanedioic acid, which was sufficient to promote viral replication ex vivo. Mechanistically, AFB1 impaired tight junction protein expression (Occludin, Claudin-1, ZO-1), reduced the expression of interferon-stimulated genes (MX1, OAS1, and ISG15), and promoted a Th17-skewed inflammatory response. Remarkably, oral supplementation with SFB reversed AFB1-mediated enhancement of H3N8 replication and ameliorated intestinal inflammation. Our findings identify a previously unrecognized mycotoxin–virus interaction axis driven by gut microbiota dysbiosis and the loss of protective SFB, highlighting AFB1 control as an urgent priority to mitigate influenza risk in poultry production.</p>

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AFB1 promotes H3N8 replication in chickens by impairing gut colonization of protective segmented filamentous bacteria

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年8月3日

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  • Zhenkai Dai,
  • Mengyue Dong,
  • Hainuo Zeng,
  • Yuhang Bai,
  • Runlin Shao,
  • Ruiheng Liu,
  • Qian Wang,
  • Jiaqian Rao,
  • Tong Li,
  • Yuanjia Liu,
  • Qingmei Xie,
  • Xinheng Zhang

摘要

Aflatoxin B1 (AFB1) is a prevalent mycotoxin in poultry feed, yet its impact on avian influenza virus H3N8 infection remains poorly understood. Here, we show that environmentally relevant concentrations of AFB1 (25–100 μg/kg) significantly enhance H3N8 replication both in chicken cell lines (DF-1 and CEF) and in specific pathogen-free (SPF) chickens. Using a multi-omics approach integrating histopathology, 16S rRNA sequencing, and untargeted metabolomics, we demonstrate that AFB1 exposure disrupts intestinal barrier integrity, induces gut dysbiosis, and specifically reduces the colonization of beneficial segmented filamentous bacteria (SFB) on the ileal epithelium. This was associated with altered lipid metabolism, notably increased levels of dodecanedioic acid, which was sufficient to promote viral replication ex vivo. Mechanistically, AFB1 impaired tight junction protein expression (Occludin, Claudin-1, ZO-1), reduced the expression of interferon-stimulated genes (MX1, OAS1, and ISG15), and promoted a Th17-skewed inflammatory response. Remarkably, oral supplementation with SFB reversed AFB1-mediated enhancement of H3N8 replication and ameliorated intestinal inflammation. Our findings identify a previously unrecognized mycotoxin–virus interaction axis driven by gut microbiota dysbiosis and the loss of protective SFB, highlighting AFB1 control as an urgent priority to mitigate influenza risk in poultry production.