适当的宿主-微生物群相互作用对于维持肠道稳态至关重要；因此，这些相互作用的不平衡会导致与炎症相关的肠道疾病。 Toll 样受体 (TLR) 识别微生物配体，并在健康和疾病的宿主-微生物相互作用中发挥关键作用。 TLR13 在增强宿主对病原菌的防御方面具有明确的功能。然而，其在维持肠道稳态和控制结肠炎相关结肠癌（CAC）方面的作用尚不清楚。本研究旨在利用离体细胞和体内 CAC 动物模型研究 TLR13 介导的信号传导在肠道稳态和结肠肿瘤发生中的参与。 Tlr13 缺陷的小鼠容易患右旋糖酐硫酸钠 (DSS) 诱导的结肠炎。在 CAC 方案（AOM/DSS 治疗）的早期阶段，Tlr13 缺乏导致严重的溃疡性结肠炎。此外，Tlr13缺陷小鼠表现出肠道通透性增加，异硫氰酸荧光素（FITC）-葡聚糖、内毒素和细菌易位水平升高证明了这一点。在 Tlr13 缺陷小鼠中观察到结肠肠细胞的细胞存活和增殖增强。转录组分析表明，Tlr13 缺陷与结肠肿瘤组织基因表达谱的实质性变化有关。 Tlr13 缺陷小鼠更容易受到 CAC 的影响，结肠组织中白细胞介素 (IL)-6、IL-12 和 TNF-α 细胞因子的产生增加，STAT3、NF-κB 和 MAPK 信号传导增强。这些发现表明 TLR13 在维持肠道稳态和控制 CAC 方面发挥保护作用。我们的研究通过 TLR13 介导的信号传导为肠道健康提供了新的视角，这对于破译宿主-微生物群相互作用在健康和疾病中的作用至关重要。© 2024 作者。约翰·威利出版的《国际癌症杂志》

Appropriate host-microbiota interactions are essential for maintaining intestinal homeostasis; hence, an imbalance in these interactions leads to inflammation-associated intestinal diseases. Toll-like receptors (TLRs) recognize microbial ligands and play a key role in host-microbe interactions in health and disease. TLR13 has a well-established function in enhancing host defenses against pathogenic bacteria. However, its role in maintaining intestinal homeostasis and controlling colitis-associated colon cancer (CAC) is largely unknown. This study aimed to investigate the involvement of TLR13-mediated signaling in intestinal homeostasis and colonic tumorigenesis using ex vivo cell and in vivo CAC animal model. Tlr13-deficient mice were prone to dextran sodium sulfate (DSS)-induced colitis. During the early stages of the CAC regimen (AOM/DSS-treated), Tlr13 deficiency led to severe ulcerative colitis. Moreover, Tlr13-deficient mice exhibited increased intestinal permeability, as evidenced by elevated levels of fluorescein isothiocyanate (FITC)-dextran, endotoxins, and bacterial translocation. Enhanced cell survival and proliferation of colonic intestinal cells were observed in Tlr13-deficient mice. A transcriptome analysis revealed that Tlr13 deficiency is associated with substantial changes in gene expression profile of colonic tumor tissue. Tlr13-deficient mice were more susceptible to CAC, with increased production of interleukin (IL)-6, IL-12, and TNF-α cytokines and enhanced STAT3, NF-κB, and MAPK signaling in colon tissues. These findings suggest that TLR13 plays a protective role in maintaining intestinal homeostasis and controlling CAC. Our study provides a novel perspective on intestinal health via TLR13-mediated signaling, which is crucial for deciphering the role of host-microbiota interactions in health and disease.© 2024 The Author(s). International Journal of Cancer published by John Wiley & Sons Ltd on behalf of UICC.