Mounting evidence suggests the impact of maternal diet on the health of offspring. We reported that maternal diet of sulforaphane glucosinolate (SGS) could prevent behavioral abnormalities in offspring after maternal immune activation. The present study was designed to investigate whether the dietary intake of SGS during pregnancy and lactation influences the composition of gut microbiota in the offspring. The dietary intake of SGS during pregnancy and lactation caused significant changes in the α-diversity and β-diversity of gut microbiota in 3-week-old offspring (SGS-3W group) and 10-week-old offspring (SGS-10W group). The LEfSe algorithm identified several microbes as important phylotypes in the SGS-3W or SGS-10W groups. Predictive functional metagenomes showed that the maternal intake of SGS caused several KEGG pathways alterations with respect to the genetic information processing and metabolism. Furthermore, the plasma levels of interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in the SGS-10W group after the injection of lipopolysaccharide (LPS: 0.5 mg/kg) were significantly lower than those of the CON-10W group. It is noteworthy that there were positive correlations between the relative abundance of the genus Blautia and IL-6 (or TNF-α) in adult offspring. Moreover, there were sex differences of gut microbiota composition in offspring. In conclusion, these data suggest that the dietary intake of SGS during pregnancy and lactation might produce long-lasting beneficial effects in adult offspring through the persistent modulation of gut microbiota. It is likely that the modulation of gut microbiota by maternal nutrition may confer resilience versus vulnerability to stress-related psychiatric disorders in the offspring.

Brain–gut–microbiota axis

Inflammation

Maternal diet

Offspring

Sex difference

Sulforaphane

Tumor necrosis factor-alpha

Kyoto encyclopedia of genes and genomics

Sulforaphane glucosinolate

Principal compotent analysis

Principal coordinate analysis

© 2022 The Author(s). Published by Elsevier Inc.