Titanium dioxide nanoparticles (TiO2 NPs) were used worldwide for decades, and pregnant women are unable to avoid exposing to them. Studies revealed that TiO2 NPs could kill many kinds of bacteria, but whether they would affect the composition of gut microbiota, especially during pregnancy, was seldom reported. And, what adverse effects may be brought to pregnant females was also unknown. In this study, we established the prenatal exposure model of rats to explore the effects of TiO2 NPs on gut microbiota. We observed an increasing trend, but not a significant change of alpha-diversity among control and exposure groups at gestation day (GD) 10 and GD 17 during normal pregnancy process. Each different time point had unique gut microbiota operational taxonomic units (OTUs) characteristics. The abundance of Ellin6075 decreased at GD 10 and GD 17, Clostridiales increased at GD 10, and Dehalobacteriaceae decreased at GD 17 after TiO2 NPs exposure. Further phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt) prediction indicated that the type 2 diabetes mellitus related genes were enhanced, and taurine metabolism was weakened at the second-trimester. Further study showed that the rats’ fasting blood glucose levels significantly increased at GD 10 (P < 0.05) and GD 17 (P < 0.01) after exposure. Our study pointed out that TiO2 NPs induced the alteration of gut microbiota during pregnancy and increased the fasting blood glucose of pregnant rats, which might increase the potential risk of gestational diabetes of pregnant women.

Scope: Supplementing Limosilactobacillus reuteri Fn041, a breast milk-derived probiotic from agricultural and pastoral areas, to maternal mice during late pregnancy and lactation prevents atopic dermatitis (AD) in offspring. This study aims to elucidate the molecular mechanism of Fn041-mediated immune regulation. Methods and results: Fn041 is administered prenatal and postnatal to maternal mice, and to offspring after weaning. The ears are administered with calcipotriol to induce AD. Fn041 treatment significantly alleviates ear inflammation, and reduces mast cell infiltration. Fn041 treatment upregulates and downregulates intestinal ZO-1 and Claudin-2 mRNA expression, respectively. Transcriptome analysis of Peyer's patches reveals that pathways related to DNA damage repair are activated in AD mice, which is inhibited by Fn041 treatment. Fn041 activates pathways related to retinol absorption and metabolism. Untargeted metabolomic analysis reveals that Fn041 treatment increases plasma retinol and kynurenine. Fn041 treatment does not significantly alter the overall cecal microbiota profile, only increases the relative abundances of Ligilactobacillus apodemi, Ligilactobacillus murinus, Akkermansia muciniphila, and Bacteroides thetaiotaomicron. Conclusions: Fn041 induces anti-AD immune responses directly by promoting the absorption and metabolism of retinol in Peyer's patches, and plays an indirect role by strengthening the mucosal barrier and increasing the abundance of specific anti-AD bacteria in the cecum.

Background Air pollution is becoming an increased burden to the world. Previous studies have confirmed its effects on adverse birth outcomes, but few associated with premature small for gestational age (SGA). We report a retrospective cohort study conducted in Changzhou city to evaluate the association between air pollutants (PM 2.5 , SO 2 and NO 2 ) and premature SGA during pregnancy. Methods A total of 46,224 births were collected from January, 2013 to December, 2016, in Changzhou Maternity and Child Health Care Hospital, finally 2709 preterm births were admitted for study. Corresponding air monitoring data were collected from Changzhou Environmental Protection Agency. Generalized estimating equations were used to examine the association between these air pollutants and premature SGA controlling for individual covariates in single- and multi-pollutant models. Results We found that, in the third trimester, every 10 μg/m 3 increments in PM 2.5 concentration were associated with premature SGA (OR = 1.18, 95% CI: 1.03–2.83; OR = 1.37, 95% CI: 1.03–3.58) in two- and three-pollutants models. In the whole gestation, a 10 μg/m 3 increment in PM 2.5 concentration in two- and three-pollutant models were related to premature SGA (OR = 1.53, 95% CI: 1.38–2.47; OR = 1.73, 95% CI: 1.18–2.57). The OR (95% CI) of premature SGA were increasing across quintiles of PM 2.5 , SO 2 , NO 2 concentrations during the whole gestation period adjusting for confounders ( P for trend < 0.001). Conclusions These results indicated that pregnant women exposed to PM 2.5, combined with other pollutants in the third trimester have a higher risk to deliver premature SGA babies, providing further evidence linking PM 2.5 and pregnancy outcomes.

Gut microbiota transmission from mother to offspring is critical to infant gut microbiota and immune development. Mother’s intestines and breast milk are rich in secretory immunoglobulin A (sIgA), which can...