Association of maternal gut microbiota with prenatal depression and the potential mediation effect by plasma tryptophan.

OBJECTIVES

Prenatal depression is one of the most common psychological disorders during pregnancy, with an incidence of approximately 19.7% in China, and the incidence is showing a significant upward trend. Prenatal depression seriously endangers maternal and infant health, may lead to self-injury and suicide, and has lasting effects on the health of offspring. Studies have shown that gut microbiota imbalance and disruption of the gut-brain axis can affect brain function and behavior and play an important role in the occurrence and development of depression. Significant changes occur in the gut microbiota of pregnant women during pregnancy, which may influence inflammation and metabolism. Gut microbiota play a key role in tryptophan metabolism; however, the mechanisms by which maternal gut microbiota regulate tryptophan metabolism to affect brain function and mood remain unclear. This study aims to clarify the role of plasma tryptophan in the relationship between gut microbiota and prenatal depression in pregnant women based on the gut-brain axis mechanism.

METHODS

A total of 73 pregnant women were included in the study. The Edinburgh Postnatal Depression Scale (EPDS) was used for assessment. According to the cutoff score (10 points), participants were divided into a prenatal depression group (pregnant women with prenatal depression) and a control group (pregnant women without prenatal depression). Demographic information, fecal samples, and plasma samples were collected. Gut microbiota sequencing was performed using 16S ribosomal RNA (rRNA) sequencing. Amino acid detection in plasma and feces was conducted using ultrahigh performance liquid chromatography-electrospray ionization tandem mass spectrometry (UHPLC-ESI-MS/MS). Data were analyzed using SPSS 26.0 and R software, and mediation model analysis was performed using SPSS PROCESS.

RESULTS

There were no statistically significant differences in α-diversity or β-diversity of gut microbiota between the 2 groups (all P>0.05). Compared with the control group, plasma tryptophan levels were significantly higher in the prenatal depression group (t=-2.964, P<0.05). The abundances of Candidatus_Soleaferrea (β=-19.945, OR<0.001, 95% CI <0.001 to 0.002, P=0.004) and Enterococcus (β=-9.074, OR<0.001, 95% CI <0.001 to 0.183, P=0.016) were negatively correlated with prenatal depression, whereas the abundance of Lachnospiraceae_NC2004_group was positively correlated with prenatal depression (β=5.870, OR=354.354, 95% CI 1.248 to 100 619.527, P=0.042). Plasma tryptophan levels played a mediating role between Enterococcus abundance and prenatal depression.

CONCLUSIONS

Depressive symptoms during pregnancy are associated with the composition of gut microbiota during pregnancy. Tryptophan, as a precursor of serotonin, may play a mediating role in this process, providing new insights for improving prenatal depression through interventions targeting gut microbiota or tryptophan metabolism.