Table_1_Metagenomic insights into the composition and function of the gut microbiota of mice infected with Toxoplasma gondii.xlsx

IntroductionDespite Toxoplasma gondii infection leading to dysbiosis and enteritis, the function of gut microbiota in toxoplasmosis has not been explored.
MethodsHere, shotgun metagenomics was employed to characterize the composition and function of mouse microbial community during acute and chronic T. gondii infection, respectively.
ResultsThe results revealed that the diversity of gut bacteria was decreased immediately after T. gondii infection, and was increased with the duration of infection. In addition, T. gondii infection led to gut microbiota dysbiosis both in acute and chronic infection periods. Therein, several signatures, including depression of Firmicutes to Bacteroidetes ratio and infection-enriched Proteobacteria, were observed in the chronic period, which may contribute to aggravated gut inflammation and disease severity. Functional analysis showed that a large amount of Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways and carbohydrate-active enzymes (CAZy) family displayed distinct variation in abundance between infected and healthy mice. The lipopolysaccharide biosynthesis related pathways were activated in the chronic infection period, which might lead to immune system imbalance and involve in intestinal inflammation. Moreover, microbial and functional spectrums were more disordered in chronic than acute infection periods, thus implying gut microbiota was more likely to participate in disease process in the chronically infected mice, even exacerbated immunologic derangement and disease progression.
DiscussionOur data indicate that the gut microbiota plays a potentially important role in protecting mice from T. gondii infection, and contributes to better understand the association between gut microbiota and toxoplasmosis.

引言 尽管刚地弓形虫（Toxoplasma gondii）感染可引发肠道菌群失调与肠炎，但目前学界尚未对肠道菌群在弓形虫病（toxoplasmosis）中的功能开展系统探究。
方法 本研究采用鸟枪宏基因组学（shotgun metagenomics）技术，分别对急性与慢性刚地弓形虫感染小鼠的肠道菌群组成及其功能进行表征分析。
结果 研究结果显示，肠道细菌的多样性在刚地弓形虫感染后即刻下降，并随感染时长的延长逐渐升高。此外，刚地弓形虫感染在急性与慢性感染阶段均会诱导肠道菌群失调。其中，慢性感染阶段可观察到多项特征性菌群异常：包括厚壁菌门/拟杆菌门比值降低以及感染富集的变形菌门，上述特征可能加剧肠道炎症反应与疾病严重程度。功能分析表明，大量京都基因与基因组百科全书（Kyoto Encyclopedia of Genes and Genomes, KEGG）通路以及碳水化合物活性酶（carbohydrate-active enzymes, CAZy）家族在感染组与健康小鼠间的丰度存在显著差异。慢性感染阶段，脂多糖生物合成相关通路被激活，这可能引发免疫系统失衡并参与肠道炎症过程。此外，慢性感染阶段的菌群与功能谱紊乱程度较急性感染阶段更为显著，提示肠道菌群更易参与慢性感染小鼠的疾病进程，甚至加剧免疫紊乱与疾病进展。
讨论 本研究数据表明，肠道菌群在小鼠抵抗刚地弓形虫感染过程中发挥潜在的重要作用，该结果有助于进一步阐明肠道菌群与弓形虫病之间的关联。