Jiangsu Key Laboratory of Immunity and Metabolism, Xuzhou Medical University, Xuzhou, 221004, Jiangsu, China.
Department of Gastroenterology, The Affiliated Shuyang Hospital of Xuzhou Medical University, No.9, Yingbin Avenue, Shuyang County, Suqian, 223600, Jiangsu, China.
BMC Gastroenterol. 2023 Oct 17;23(1):358. doi: 10.1186/s12876-023-02971-5.
The aim of this study was to explore the mechanism whereby LACC1 regulates the intestinal flora in a mouse model of inflammatory bowel disease (IBD).
C57BL/6 and Lacc1 mice were used to establish a mouse model of IBD induced by dextran sodium sulfate (DSS). The effects of Lacc1 deletion in mice were evaluated. Changes in the body weight and stool blood were recorded daily. After 7 days of successful modeling, the mice were sacrificed, blood was collected from the eyeballs, the entire colon was dissected and separated, and the length of the colon was measured.
Compared with the wild-type (WT) DSS model group, the Lacc1 DSS model group showed a significantly higher disease activity index score (P < 0.05), significantly faster weight loss (P < 0.05), and a significantly shorter colon (P < 0.05), indicating that the colonic mucosal tissue was seriously damaged in the Lacc1 DSS model group (P < 0.05). Serum IL-1β, IL-6, TNF-α, and IFN-γ levels were significantly higher in the Lacc1 DSS model group than the WT DSS model group. Principal coordinate analysis showed that there were significant microbiome differences between the WT, Lacc1, WT DSS model, and Lacc1 DSS model groups (P < 0.05). Linear discriminant analysis effect size analysis showed that under natural conditions, Lacc1 mice had significant changes in their intestinal flora compared with control mice (LDA value > 3 or < 3, P < 0.05).
Lacc1 deletion aggravates DSS-induced IBD in mice.
本研究旨在探讨 LACC1 通过何种机制调节炎症性肠病（IBD）小鼠模型中的肠道菌群。
采用 C57BL/6 和 Lacc1 小鼠建立葡聚糖硫酸钠（DSS）诱导的 IBD 小鼠模型，评估 Lacc1 缺失对小鼠的影响。每天记录体重和粪便潜血变化。造模 7 天后处死小鼠，眼球采血，分离并取出整个结肠，测量结肠长度。
与野生型（WT）DSS 模型组相比，Lacc1 DSS 模型组疾病活动指数评分更高（P<0.05），体重下降更快（P<0.05），结肠更短（P<0.05），提示 Lacc1 DSS 模型组结肠黏膜组织损伤严重（P<0.05）。Lacc1 DSS 模型组血清白细胞介素 1β（IL-1β）、白细胞介素 6（IL-6）、肿瘤坏死因子-α（TNF-α）和干扰素-γ（IFN-γ）水平均明显高于 WT DSS 模型组。主坐标分析显示，WT、Lacc1、WT DSS 模型组和 Lacc1 DSS 模型组之间的微生物组存在显著差异（P<0.05）。线性判别分析效应量分析显示，在自然条件下，Lacc1 小鼠的肠道菌群与对照小鼠相比有显著变化（LDA 值>3 或<3，P<0.05）。
Lacc1 缺失加重了 DSS 诱导的 IBD 小鼠模型的病情。
