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母羊多房棘球绦虫感染对后代结肠炎易感性和肠道微生物群的影响。

Effects of maternal Echinococcus multilocularis infection on colitis susceptibility and gut microbiota of offspring.

作者信息

Liu Yihui, Xu Yang, Zou Yang, Ding Yingying, Zhang Jiayun, Zhang Ying, Pang Quanhai, Wang Shuai

机构信息

College of Veterinary Medicine, Shanxi Agricultural University, Taigu, 030801, Shanxi, China.

State Key Laboratory of Animal Disease Control and Prevention, College of Veterinary Medicine, Lanzhou University, Lanzhou Veterinary Research Institute, Chinese Academy of Agricultural Sciences, Lanzhou, 730000, Gansu, China.

出版信息

Parasit Vectors. 2025 Jul 26;18(1):299. doi: 10.1186/s13071-025-06915-8.

DOI:10.1186/s13071-025-06915-8
PMID:40713878
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12297764/
Abstract

BACKGROUND

Maternal immune modulation and alterations in gut microbiota due to intestinal helminth infections may be passed on to offspring. However, it remains unclear whether these effects can be transferred between maternal mice and their offspring during tissue-dwelling helminth infections.

METHODS

In this study, we investigated the effect of maternal infection with Echinococcus multilocularis (Emu) on offspring susceptibility to colitis and gut microbiota composition using a dextran sulfate sodium (DSS)-induced colitis model. We performed 16S ribosomal RNA (rRNA) sequencing to analyze the gut microbiota composition and microbial abundance in Emu-infected and control maternal mice, as well as their offspring.

RESULTS

We found that the maternal mice infected with Emu exhibited significant resistance to colitis, characterized by increased expression of Foxp3 in colonic tissue. Conversely, this resistance phenotype was not observed in the offspring of Emu-infected maternal mice, as they showed no reduction in colitis severity and demonstrated decreased Foxp3 expression. Furthermore, the gut microbiota of Emu-infected maternal mice underwent significant changes, with an increase in genera such as Rikenella, Rikenellaceae RC9 gut group, Turicibacter, Odoribacter, and Parabacteroides, while Lactobacillus, Staphylococcus, and Bifidobacterium decreased postinfection. By contrast, their offspring exhibited a markedly distinct gut microbiota shift, characterized by significant increases in Candidatus Saccharimonas, Desulfovibrio, Helicobacter, and Odoribacter, alongside significant reductions in Muribaculum and Clostridium sensu stricto 1 when compared with the offspring of naive mice.

CONCLUSIONS

These findings suggest that the effects of maternal transmission concerning immune regulation and microbiota alterations in response to helminth infections may depend on species-specific factors.

摘要

背景

肠道蠕虫感染导致的母体免疫调节和肠道微生物群改变可能会传递给后代。然而,在组织内寄生蠕虫感染期间,这些影响是否能在母鼠及其后代之间传递仍不清楚。

方法

在本研究中,我们使用葡聚糖硫酸钠(DSS)诱导的结肠炎模型,研究了多房棘球绦虫(Emu)母体感染对后代结肠炎易感性和肠道微生物群组成的影响。我们进行了16S核糖体RNA(rRNA)测序,以分析Emu感染和对照母鼠及其后代的肠道微生物群组成和微生物丰度。

结果

我们发现,感染Emu的母鼠对结肠炎表现出显著抗性,其特征是结肠组织中Foxp3表达增加。相反,在感染Emu的母鼠后代中未观察到这种抗性表型,因为它们的结肠炎严重程度没有降低,且Foxp3表达降低。此外,感染Emu的母鼠肠道微生物群发生了显著变化,Rikenella、Rikenellaceae RC9肠道菌群、Turicibacter、Odoribacter和Parabacteroides等属增加,而感染后乳酸杆菌、葡萄球菌和双歧杆菌减少。相比之下,与未感染母鼠的后代相比,它们的后代肠道微生物群发生了明显不同的变化,特征是假单胞菌属、脱硫弧菌属、螺杆菌属和Odoribacter显著增加,同时Muribaculum和严格意义上的梭菌属1显著减少。

结论

这些发现表明,母体传播对蠕虫感染的免疫调节和微生物群改变的影响可能取决于物种特异性因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2c7/12297764/5898ad8822e8/13071_2025_6915_Fig5_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2c7/12297764/5898ad8822e8/13071_2025_6915_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2c7/12297764/e24062bfe6e6/13071_2025_6915_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2c7/12297764/81db85f0e4a3/13071_2025_6915_Fig2_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/e2c7/12297764/99e3325c2f02/13071_2025_6915_Fig4_HTML.jpg
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本文引用的文献

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Helminth reshapes host gut microbiota and immunoregulation by deploying an antimicrobial program of innate immunity.蠕虫通过启动先天性免疫的抗菌程序来重塑宿主肠道微生物群和免疫调节。
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serpin regulates macrophage polarization and reduces gut dysbiosis in colitis.丝氨酸蛋白酶抑制剂调节巨噬细胞极化,减少结肠炎中的肠道菌群失调。
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Interaction between tissue-dwelling helminth and the gut microbiota drives mucosal immunoregulation.
组织内寄生虫与肠道微生物群的相互作用驱动黏膜免疫调节。
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Maternal helminth infection protects offspring from high-fat-diet-induced obesity through altered microbiota and SCFAs.母体寄生虫感染通过改变微生物群和短链脂肪酸来保护后代免受高脂肪饮食诱导的肥胖。
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