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观察 ANKA 感染诱导的 C57BL/6 小鼠肠道微生物群特征。

Observation of the Gut Microbiota Profile in C57BL/6 Mice Induced by ANKA Infection.

机构信息

Department of Human Parasitology, School of Basic Medicine, Hubei University of Medicine, Shiyan, China.

Department of Infectious Diseases, Renmin Hospital, Hubei University of Medicine, Shiyan, China.

出版信息

Front Cell Infect Microbiol. 2021 Oct 28;11:680383. doi: 10.3389/fcimb.2021.680383. eCollection 2021.

DOI:10.3389/fcimb.2021.680383
PMID:34778098
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC8581563/
Abstract

The genus of parasites can cause malaria, which is a prevalent infectious disease worldwide, especially in tropical and subtropical regions. C57BL/6 mice infected with ANKA (PbA) will suffer from experimental cerebral malaria (ECM). However, the gut microbiota in C57BL/6 mice has rarely been investigated, especially regarding changes in the intestinal environment caused by infectious parasites. ANKA-infected (PbA group) and uninfected C57BL/6 (Ctrl group) mice were used in this study. C57BL/6 mice were infected with PbA intraperitoneal injection of 1 × 10 infected red blood cells. Fecal samples of two groups were collected. The microbiota of feces obtained from both uninfected and infected mice was characterized by targeting the V4 region of the 16S rRNA through the Illumina MiSeq platform. The variations in the total gut microbiota composition were determined based on alpha and beta diversity analyses of 16S rRNA sequencing. The raw sequences from all samples were generated and clustered using ≥ 97% sequence identity into many microbial operational taxonomic units (OTUs). The typical microbiota composition in the gut was dominated by , , , and at the phylum level. and were considerably decreased after PbA infection compared with the control group (Ctrl), while and were increased substantially after PbA infection compared with Ctrl. The alpha diversity index showed that the observed OTU number was increased in the PbA group compared with the Ctrl group. Moreover, the discreteness of the beta diversity revealed that the PbA group samples had a higher number of OTUs than the Ctrl group. LEfSe analysis revealed that several potential bacterial biomarkers were clearly related to the PbA-infected mice at the phylogenetic level. Several bacterial genera, such as , , and , were overrepresented in the PbAinfected fecal microbiota. Meanwhile, a method similar to gene coexpression network construction was used to generate the OTU co-abundance units. These results indicated that ANKA infection could alter the gut microbiota composition of C57BL/6 mice. In addition, potential biomarkers should offer insight into malaria pathogenesis and antimalarial drug and malaria vaccine studies.

摘要

寄生虫属可引起疟疾,这是一种全球流行的传染病,尤其在热带和亚热带地区。用 ANKA(PbA)感染 C57BL/6 小鼠会导致实验性脑型疟疾(ECM)。然而,C57BL/6 小鼠的肠道微生物群很少被研究,特别是关于感染寄生虫引起的肠道环境变化。本研究使用了 ANKA 感染(PbA 组)和未感染 C57BL/6(Ctrl 组)的小鼠。通过腹腔注射 1×10 个感染的红细胞将 PbA 感染 C57BL/6 小鼠。收集两组的粪便样本。通过 Illumina MiSeq 平台靶向 16S rRNA 的 V4 区,对来自未感染和感染小鼠的粪便微生物群进行了特征描述。基于 16S rRNA 测序的α和β多样性分析,确定了总肠道微生物群组成的变化。从所有样本中生成的原始序列使用≥97%的序列同一性聚类成许多微生物操作分类单元(OTU)。肠道中的典型微生物群组成在门水平上主要由 、 、 和 主导。与对照组(Ctrl)相比,PbA 感染后 和 显著减少,而 和 显著增加。α多样性指数显示,与对照组相比,PbA 组的观察到的 OTU 数量增加。此外,β多样性的离散性表明,PbA 组样本的 OTU 数量高于对照组。LEfSe 分析表明,在系统发育水平上,一些潜在的细菌生物标志物与 PbA 感染的小鼠明显相关。在 PbA 感染的粪便微生物群中,一些细菌属,如 、 和 等,过度表达。同时,使用类似于基因共表达网络构建的方法生成 OTU 共丰度单位。这些结果表明,ANKA 感染可改变 C57BL/6 小鼠的肠道微生物群组成。此外,潜在的生物标志物应该为疟疾发病机制以及抗疟药物和疟疾疫苗研究提供新的见解。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c31/8581563/0e6a71724a0e/fcimb-11-680383-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c31/8581563/aa6b5e789cf8/fcimb-11-680383-g001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c31/8581563/b10fe677afb7/fcimb-11-680383-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c31/8581563/0e6a71724a0e/fcimb-11-680383-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c31/8581563/aa6b5e789cf8/fcimb-11-680383-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c31/8581563/819547538258/fcimb-11-680383-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c31/8581563/986f4aa0af8d/fcimb-11-680383-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c31/8581563/b10fe677afb7/fcimb-11-680383-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/6c31/8581563/0e6a71724a0e/fcimb-11-680383-g005.jpg

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