The Relationship Between Maternal and Neonatal Microbiota in Spontaneous Preterm Birth: A Pilot Study

Abstract

The newborn’s microbiota composition at birth seems to be influenced by maternal microbiota. Maternal vaginal microbiota can be a determining factor of spontaneous Preterm Birth (SPPTB), the leading cause of perinatal mortality. The aim of the study is to investigate the likelihood of a causal relationship between the maternal vaginal microbiota composition and neonatal lung and intestinal microbiota profile at birth, in cases of SPPTB. The association between the lung and/or meconium microbiota with the subsequent development of bronchopulmonary dysplasia (BPD) was also investigated. Maternal vaginal swabs, newborns’ bronchoalveolar lavage fluid (BALF) (1st, 3rd, 7th day of life) and first meconium samples were collected from 20 women and 23 preterm newborns with gestational age ≤ 30 weeks (12 = SPPTB; 11 = Medically Indicated Preterm Birth–MIPTB). All the samples were analyzed for culture examination and for microbiota profiling using metagenomic analysis based on the Next Generation Sequencing (NGS) technique of the bacterial 16S rRNA gene amplicons. No significant differences in alpha e beta diversity were found between the neonatal BALF samples of SPPTB group and the MIPTB group. The vaginal microbiota of mothers with SPPTB showed a significant difference in alpha diversity with a decrease in Lactobacillus and an increase in Proteobacteria abundance. No association was found between BALF and meconium microbiota with the development of BPD. Vaginal colonization by Ureaplasma bacteria was associated with increased risk of both SPPTB and newborns’ BPD occurrence. In conclusion, an increase in α-diversity values and a consequent fall in Lactobacillus in vaginal environment could be associated to a higher risk of SPPTB. We could identify neither a specific neonatal lung or meconium microbiota profiles in preterm infants born by SPPTB nor a microbiota at birth suggestive of subsequent BPD development. Although a strict match has not been revealed between microbiota of SPPTB mother-infant couples, a relationship cannot be excluded. To figure out the reciprocal influence of the maternal-neonatal microbiota and its potential role in the pathogenesis of SPPTB and BPD further research is needed.

Preterm Infants’ Airway Microbiome: A Scoping Review of the Current Evidence

“…Specifically, at the time of intubation, premature infants who developed BPD had lower bacterial diversity than those who did not develop BPD, as estimated by the number of observed species and the Shannon diversity index. This finding is supported by Tirone et al [ 28 ] who also observed a slight reduction, although not statistically significant, in the Shannon diversity index in BALF samples from infants with BPD. Tirone and colleagues did not identify a characteristic microbiological signature linked to BPD development at either the genus or phylum level.…”

“…Tirone et al [ 28 ] demonstrated that, while the vaginal microbiota of mothers with a spontaneous preterm birth (SP PTB ) showed a significant difference in alpha diversity, marked by a decrease in Lactobacillus and an increase in Proteobacteria abundance, there were no significant differences in alpha e beta diversity between the neonatal bronchoalveolar lavage fluid (BALF) samples of the SP PTB group and the medically indicated preterm birth (MI PTB ) group. Regarding chorioamnionitis, Lohman et al [ 1 ] also reported that there were no statistically significant differences in bacterial diversity in endotracheal aspiration samples from newborns with and without exposure to chorioamnionitis, although they noted a trend toward decreased diversity in those infants who had been exposed.…”

“…The findings suggest the possibility of a complex interplay between microbial diversity, composition, and the risk of BPD, even if this should still be clarified. In some of the included studies, infants diagnosed with BPD exhibit distinct microbial evolution patterns, marked by lower diversity at the time of intubation [ 1 , 20 , 28 , 29 ] and variations in phylum-level abundance [ 1 , 24 , 26 , 34 ], but the impact of these variations on clinical management needs further clarification. The prevalence of specific genera, such as Ureaplasma , stands out as potential indicators of BPD risk; the causal relationship between organism and disease also may need further investigation.…”

Analysis of Vaginal Microbiota Variations in the Third Trimester of Pregnancy and Their Correlation with Preterm Birth: A Case-Control Study

“…Despite advances in neonatal care, the rates of preterm births have not significantly decreased worldwide in recent years, highlighting the need for a deeper understanding of its etiology [ 3 , 4 ]. Emerging research has increasingly pointed to the role of the vaginal microbiota in maternal and neonatal health, suggesting a significant association between microbial dysbiosis and adverse pregnancy outcomes, including preterm birth [ 5 , 6 ]. The vaginal microbiome, a complex ecosystem of bacteria, varies widely among women and changes throughout pregnancy, influenced by factors such as genetics, environment, and lifestyle [ 7 , 8 ].…”

Gut microbiota in women: The secret of psychological and physical well-being

“…During pregnancy, the gut microbiota primarily defends the health of the mother, for example, by helping her not to develop gestational diabetes, and at the same time, it also preserves that of the child who will be exposed to the first “transfer” of microorganisms at the time of birth[ 32 ]. The vertical transmission of the microbiota from mother to fetus, which appears to begin during intrauterine life, contributes to the development of the child’s gastrointestinal microbiota[ 33 ]. Going toward the third trimester, the relative abundance of some bacteria that are then transferred to the newborn in the peripartum (in the case of vaginal birth) increases: In fact, the child’s gut microbiota consists of 22% bacteria derived from the mother’s gut microbiota, particularly Bifidobacteria , Bacteroides , and Escherichia coli [ 31 ].…”