Gut microbiota from women with prenatal depression induced depressive-like behavior and hippocampal inflammatory signals in germ-free mice.
Evidence
This experiment combined germ-free mouse behavior, metagenomics, metabolomics, plasma LPS, and hippocampal neuroinflammation markers.
Caveat
The evidence comes from a mouse transfer model, so it supports a possible microbiota-driven mechanism rather than direct proof of the pathway in pregnant humans.
Simplified
Numerous studies have described the role of the microbiome-gut-brain axis in depression. However, the molecular mechanisms underlying the involvement of gut microbiota in the development of prenatal depression are limited. In this study, fecal microbiota from women with prenatal depression was transplanted into germ-free mice to investigate the potential causal relationships between the gut microbiota and depressive phenotypes. Shotgun metagenomic sequencing and untargeted metabolomics approaches were used to investigate the characteristics of gut microbiota and microbial metabolites. The levels of neuroinflammation in the brain were detected using immunofluorescence and real-time quantitative PCR. We found significant changes in gut microbiota composition and metabolites in mice with (FMT) from women with prenatal depression, including decreased Ligilactobacillus, increased Akkermansia, and abnormal glycerophospholipid metabolism. Besides, significant increase in plasma lipopolysaccharide (LPS) levels and significant proliferation of microglia in the hippocampus were observed in mice receiving FMT from women with prenatal depression, accompanied by a significant increase in the expression of nuclear factor-κB (NF-κB) p65, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) mRNA. The gut microbiota and its metabolites were strongly associated with depressive-like behaviors, plasma LPS and neuroinflammation. Our study collectively demonstrates that dysbiosis of the gut microbiota may play a causal relationship in the development of prenatal depression. This process potentially involves the activation of neuroinflammation through the LPS-NF-κB signaling pathway.
Key numbers
17×
Increase in Akkermansia
Relative abundance of Akkermansia in the gut microbiota of recipient mice.
17×
Decrease in Ligilactobacillus
Relative abundance of Ligilactobacillus in the gut microbiota of recipient mice.
17×
Increase in plasma
Plasma concentrations in recipient mice.
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