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探讨乳杆菌 CIDCA 133 后生元蛋白对炎症性肠病模型的抗炎作用。

Exploring the anti-inflammatory effects of postbiotic proteins from Lactobacillus delbrueckii CIDCA 133 on inflammatory bowel disease model.

机构信息

Federal University of Minas Gerais, Department of Genetics, Ecology, and Evolution, Belo Horizonte, Minas Gerais, Brazil.

Federal University of Minas Gerais, Department of Clinical and Toxicological Analysis, Belo Horizonte, Minas Gerais, Brazil.

出版信息

Int J Biol Macromol. 2024 Oct;277(Pt 2):134216. doi: 10.1016/j.ijbiomac.2024.134216. Epub 2024 Jul 26.

DOI:10.1016/j.ijbiomac.2024.134216
PMID:39069058
Abstract

Lactobacillus delbrueckii CIDCA 133 is a promising health-promoting bacterium shown to alleviate intestinal inflammation. However, the specific bacterial components responsible for these effects remain largely unknown. Here, we demonstrated that consuming extractable proteins from the CIDCA 133 strain effectively relieved acute ulcerative colitis in mice. This postbiotic protein fraction reduced the disease activity index and prevented colon shortening in mice. Furthermore, histological analysis revealed colitis prevention with reduced inflammatory cell infiltration into the colon mucosa. Postbiotic consumption also induced an immunomodulatory profile in colitic mice, as evidenced by both mRNA transcript levels (Tlr2, Nfkb1, Nlpr3, Tnf, and Il6) and cytokines concentration (IL1β, TGFβ, and IL10). Additionally, it enhanced the levels of secretory IgA, upregulated the transcript levels of tight junction proteins (Hp and F11r), and improved paracellular intestinal permeability. More interestingly, the consumption of postbiotic proteins modulated the gut microbiota (Bacteroides, Arkkemansia, Dorea, and Oscillospira). Pearson correlation analysis indicated that IL10 and IL1β levels were positively associated with Bacteroides and Arkkemansia_Lactobacillus abundance. Our study reveals that CIDCA 133-derived proteins possess anti-inflammatory properties in colonic inflammation.

摘要

德氏乳杆菌 CIDCA 133 是一种有潜力的促健康细菌,已被证明可以缓解肠道炎症。然而,负责这些作用的特定细菌成分在很大程度上仍然未知。在这里,我们证明了消耗 CIDCA 133 菌株的可提取蛋白可以有效缓解小鼠的急性溃疡性结肠炎。这种后生蛋白部分降低了疾病活动指数并防止了小鼠的结肠缩短。此外,组织学分析显示,后生蛋白的消耗可预防结肠炎,减少了结肠黏膜中的炎症细胞浸润。后生蛋白的消耗还诱导了结肠炎小鼠的免疫调节特征,这表现在 mRNA 转录水平(Tlr2、Nfkb1、Nlpr3、Tnf 和 Il6)和细胞因子浓度(IL1β、TGFβ 和 IL10)上。此外,它增强了分泌型 IgA 的水平,上调了紧密连接蛋白(Hp 和 F11r)的转录水平,并改善了细胞旁肠通透性。更有趣的是,后生蛋白的消耗调节了肠道微生物群(拟杆菌、阿克曼氏菌、多拉菌和颤螺旋菌)。Pearson 相关分析表明,IL10 和 IL1β 水平与拟杆菌和阿克曼氏菌-乳酸菌的丰度呈正相关。我们的研究表明,CIDCA 133 衍生的蛋白在结肠炎症中具有抗炎特性。

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