The disruption of intestinal homeostasis when foods are colored red.
The disruption of intestinal homeostasis when foods are colored red.
复制标题
当食物呈红色时，肠道稳态会受到破坏。
DOI：
10.1038/s41423-022-00875-0
复制
发表时间：
2022
影响因子：
24.1
通讯作者：
Cong,Yingzi
中科院分区：
文献类型：
--
作者：
Yang,Wenjing;Cong,Yingzi
食品着色剂 Red 40 已被证明会在 IL-23 失调的情况下诱发结肠炎。然而，所涉及的机制仍不完全清楚。陈等人的一项研究。在本期《细胞分子免疫学》中 [1] 表明，在骨髓细胞产生 IL-23 失调的情况下，Red 40 会诱导 IFNγ+ 细胞毒性 CD4+ T 细胞，从而促进结肠炎。众所周知，炎症性肠病（IBD）的发病机制涉及遗传易感个体对肠道微生物群的粘膜免疫反应失调[2]。全基因组关联研究 (GWAS) 已确定了 200 多个 IBD 风险位点，其中一些风险位点已在各种结肠炎动物模型中进行了评估 [3]。然而，所有这些基因/位点的组合仅占疾病遗传力的一小部分，这表明环境因素在 IBD 的发病机制中也发挥着关键作用。越来越多的证据表明，各种免疫细胞类型通过细胞因子介导的细胞间通讯协调其功能，从而调节IBD的发病机制[4]。 IL-23 是由 IL12p40 和 IL23p19 组成的异二聚体。它主要由先天骨髓细胞产生并作用于 Th17 细胞，这对于介导 IBD 的发病机制至关重要 [5]。 IL23R 中的编码变异与预防 IBD 发病相关，而编码 IL-12p40 的 IL12B 基因座与 IBD 风险相关[6]。然而，在动物模型中，骨髓细胞中单独过度表达 IL-23 不会引起结肠炎，这表明包括局部环境变量在内的其他因素可以协调疾病的发展。 除了深刻影响肠道稳态和 IBD 的肠道微生物群外，某些饮食成分已被证明会影响 IBD 的发病机制。饮食可以通过多种机制调节 IBD 发病率，例如对宿主细胞的直接作用或改变肠道微生物群的间接作用 [7]。由石油制成并经美国食品和药物管理局 (FDA) 批准用于增强加工食品颜色的人造食品着色剂广泛应用于食品和制药行业。最流行的食用色素是 Red 40（也称为 Allura Red AC）、Yellow 5 和 Yellow 6。这三种着色剂占美国使用的所有食用色素的 90%，并且存在于许多食品、饮料和药品中 [8]。尽管据报道它们对宿主没有不利的细胞毒性作用，但它们是否以及如何影响人类疾病（包括IBD）仍不清楚。陈等人的一项优雅的研究。本期《细胞分子免疫学》[1] 证明，在骨髓细胞大量产生 IL-23 的情况下，Red 40 诱导 IFNγ+ 细胞毒性 CD4+ T 细胞引起结肠炎。在之前的研究中，同一小组通过以下方法培育了一种小鼠品系：
Food colorant Red 40 has been shown to induce colitis in the context of dysregulated IL-23. However, the mechanism involved is still not fully understood. A study by Chen et al. in this issue of Cellular Molecular Immunology [1] demonstrates that under dysregulated IL-23 production from myeloid cells, Red 40 induces IFNγ+ cytotoxic CD4+ T cells to promote colitis. It is well established that the pathogenesis of inflammatory bowel diseases (IBD) involves dysregulated mucosal immune responses to gut microbiota in genetically susceptible individuals [2]. Over 200 risk loci for IBD have been identified by genome-wide association studies (GWAS), and some of these risk loci have been evaluated in various animal models of colitis [3]. However, the combination of all these genes/loci only accounts for a small proportion of disease heritability, suggesting that environmental factors also play a critical role in the pathogenesis of IBD. Accumulating evidence has revealed that various immune cell types coordinate their functions through cytokine-mediated intercellular communication to regulate the pathogenesis of IBD [4]. IL-23 is a heterodimer that is comprised of IL12p40 and IL23p19. It is primarily produced by innate myeloid cells and acts on Th17 cells, which are crucial in mediating the pathogenesis of IBD [5]. The coding variants in IL23R are associated with protection from IBD onset, and the IL12B locus, which encodes IL-12p40, is associated with IBD risk [6]. However, overexpression of IL-23 alone in myeloid cells does not cause colitis in animal models, indicating that other factors, including local environmental variables, coordinate disease development.In addition to the gut microbiota, which profoundly affects intestinal homeostasis and IBD, certain dietary components have been shown to influence the pathogenesis of IBDs. The diet could regulate IBD incidence through various mechanisms, such as direct actions on host cells or indirect actions that alter the gut microbiota [7]. Artificial food colorants that are made from petroleum and approved by the US Food and Drug Administration (FDA) to enhance the color of processed foods are widely used in the food and pharmaceutical industries. The most popular food colorants are Red 40 (also known as Allura Red AC), Yellow 5, and Yellow 6. These three colorants make up 90% of all the food dyes used in the US and are found in many foods, beverages, and medicines [8]. Although they are reported to have no adverse cytotoxic effect on the host, whether and how they affect human diseases, including IBD, is still unclear. An elegant study by Chen et al. in this issue of Cellular Molecular Immunology [1] demonstrated that under high IL-23 production from myeloid cells, Red 40 induced IFNγ+ cytotoxic CD4+ T cells to cause colitis. In previous studies, the same group developed a strain of mice by