Autophagy‐related 16‐like 1 (Atg16l1) contributes to the susceptibility to ulcerative colitis (UC). The functional consequences of Atg16l1 in UC pathogenesis are poorly understood. We aimed to confirm how Atg16l1 deficiency in dendritic cells (DCs) affects murine colitis development. Atg16l1f/f mice and mice with Atg16l1 deficiency in CD11c+DCs (Atg16l1ΔDC) were generated for colitis models induction. Disease activity index, weight loss, colon score/length, and histopathological analysis were assessed for colitis severity. Mononuclear cells from mesenteric lymph node (MLN) were extracted for CD44/CD69 measurement by flow cytometry. Bacterial cultures of MLN and stool homogenates were used to evaluate the bacterial translocation. Bone marrow‐derived dendritic cells (BMDCs) were isolated and cultured for immunofluorescence of autophagy‐related proteins. Atg16l1 knockout in CD11c+DCs exacerbated intestinal inflammation of dextran sulfate sodium (DSS)‐induced colitis in vivo. Atg16l1 deficiency in CD11c+DCs had no effect on the expression of CD44 and CD69. Bacterial translocation showed that bacteria amount in MLN and stool of DSS‐induced colitis with Atg16l1 deficiency significantly higher than that of control. Immunofluorescence revealed that Atg16l1 deficiency obviously inhibited co‐expression of LC3 and Lamp1 with S. typhimurium, enhanced co‐expression of rab5 and rab7 with S. typhimurium, while did not affect Beclin1. We confirmed that Atg16l1 deficiency in DCs exacerbated the intestinal inflammation of DSS‐induced colitis. Atg16l1 deficiency in DCs promotes the bacterial translocation of DSS‐induced colitis in vivo and regulates autophagy and phagocytosis in BMDCs. Findings provided a novel perspective to study UC pathogenesis.

中文翻译：

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树突状细胞中的 Atg16l1 是鼠结肠炎抗菌防御和自噬所必需的

自噬相关的 16-like 1 (Atg16l1) 有助于溃疡性结肠炎 (UC) 的易感性。Atg16l1 在 UC 发病机制中的功能后果知之甚少。我们旨在确认树突状细胞 (DC) 中 Atg16l1 缺乏如何影响小鼠结肠炎的发展。生成 Atg16l1f/f 小鼠和 CD11c+DC 中 Atg16l1 缺陷的小鼠 (Atg16l1ΔDC) 用于结肠炎模型诱导。评估疾病活动指数、体重减轻、结肠评分/长度和组织病理学分析的结肠炎严重程度。从肠系膜淋巴结 (MLN) 中提取单核细胞用于通过流式细胞术测量 CD44/CD69。MLN 和粪便匀浆的细菌培养物用于评估细菌易位。骨髓来源的树突细胞（BMDCs）被分离和培养用于自噬相关蛋白的免疫荧光。CD11c+DCs 中的 Atg16l1 敲除加剧了葡聚糖硫酸钠（DSS）诱导的体内结肠炎的肠道炎症。CD11c+DC 中的 Atg16l1 缺陷对 CD44 和 CD69 的表达没有影响。细菌易位显示，在 DSS 诱导的 Atg16l1 缺陷结肠炎的 MLN 和粪便中细菌数量显着高于对照。免疫荧光显示，Atg16l1 缺乏明显抑制 LC3 和 Lamp1 与 S. typhimurium 的共表达，增强 rab5 和 rab7 与 S. typhimurium 的共表达，而对 Beclin1 没有影响。我们证实 DCs 中的 Atg16l1 缺乏加剧了 DSS 诱导的结肠炎的肠道炎症。DCs 中的 Atg16l1 缺陷促进了 DSS 诱导的体内结肠炎的细菌易位，并调节了 BMDCs 的自噬和吞噬作用。研究结果为研究 UC 发病机制提供了新的视角。