肠道渗透性、肠道炎症和肠道免疫系统反应与肠道微生物群组成中与衰老相关的变化有关:一项对雌性小鼠的研究。

Paola Elizabeth Gámez-Macías, Elisa Félix-Soriano, Mirian Samblas, Neira Sáinz, María Jesús Moreno-Aliaga, Pedro González-Muniesa
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引用次数: 0

摘要

衰老会导致细胞层面的变化,从而增加各种病变的风险。肠道微生物群与年龄相关疾病之间也有关联。本研究旨在分析粪便微生物群组成的变化及其与免疫反应、肠道炎症和肠道屏障损伤相关基因的关系。研究人员分析了不同年龄段(2 个月、6 个月、12 个月和 18 个月)雌性小鼠的粪便样本以及结肠组织中的基因表达。结果显示,年龄较大的小鼠组比年龄较小的小鼠组拥有更多样化的微生物群。此外,随着年龄的增长,蓝细菌属、变形菌属、黄杆菌科、乳杆菌属、副乳杆菌属、Prevotellaceae_UCG-001、Akkermansia 和 Parabacteroides goldsteinii 的丰度也在增加。相反,梭状芽孢杆菌科(Clostridiaceae)、乳酸菌科(Lactobacillaceae)、单胞菌科(Monoglobaceae)、ligilactobacillus、Limosilactobacillus、Mucispirillum 和 Bacteroides faecichinchillae 的数量明显减少。这些细菌的失衡与结肠中炎症标志物(包括 Tnf-α、Ccl2 和 Ccl12)的增加呈正相关,与紧密连接基因(Jam2、Tjp1 和 Tjp2)以及免疫反应基因(Cd4、Cd72、Tlr7、Tlr12 和 Lbp)的表达呈负相关。总之,高水平的多样性并不会改善老年小鼠的健康状况;然而,随着衰老而出现的细菌丰度失衡可能会导致免疫衰老、炎症和肠漏疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Intestinal Permeability, Gut Inflammation, and Gut Immune System Response Are Linked to Aging-Related Changes in Gut Microbiota Composition: A Study in Female Mice.

Aging entails changes at the cellular level that increase the risk of various pathologies. An association between gut microbiota and age-related diseases has also been attributed. This study aims to analyze changes in fecal microbiota composition and their association with genes related to immune response, gut inflammation, and intestinal barrier impairment. Fecal samples of female mice at different ages (2 months, 6 months, 12 months, and 18 months) and gene expression in colon tissue were analyzed. Results showed that the older mice group had a more diverse microbiota than the younger group. Additionally, the abundance of Cyanobacteria, Proteobacteria, Flavobacteriaceae, Bacteroides, Parabacteroides, Prevotellaceae_UCG-001, Akkermansia, and Parabacteroides goldsteinii increased with age. In contrast, there was a notable decline in Clostridiaceae, Lactobacillaceae, Monoglobaceae, Ligilactobacillus, Limosilactobacillus, Mucispirillum, and Bacteroides faecichinchillae. These bacteria imbalances were positively correlated with increased inflammation markers in the colon, including Tnf-α, Ccl2, and Ccl12, and negatively with the expression of tight junction genes (Jam2, Tjp1, and Tjp2), as well as immune response genes (Cd4, Cd72, Tlr7, Tlr12, and Lbp). In conclusion, high levels of diversity did not result in improved health in older mice; however, the imbalance in bacteria abundance that occurs with aging might contribute to immune senescence, inflammation, and leaky gut disease.

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