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

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.

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.

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.

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.