Maternal Gut Microbiota Research Articles

Association Between Gut Microbiota and Insulin Therapy in Women With Gestational Diabetes Mellitus

ObjectivesAt the time of diagnosis, the blood glucose of women with gestational diabetes mellitus (GDM) who require subsequent insulin treatment does not differ from that of women with adequate diet control. Hence, in this study, we aimed to determine the role of maternal gut microbiota as a marker of insulin necessity in GDM and to identify the effect of insulin therapy on gut microbiota composition in mothers with GDM and their newborns. MethodsSeventy-one pregnant women were enrolled into the study, including 38 GDM and 33 non-GDM participants. During the follow-up period, 8 of the 38 GDM subjects required insulin therapy (GDM-I group), whereas 30 of the 38 GDM cases with sufficient glycemic control by diet alone (GDM-D group). Maternal blood and feces were obtained at the time of GDM diagnosis (pretreatment; 24 to 28 weeks of gestation) and before delivery (posttreatment; ≥37 weeks of gestation). Meconium and first feces of the newborns were also collected. ResultsPretreatment, the glycemic profile did not differ between the GDM-D and GDM-I groups. However, the proportions of Clostridiales, Lactobacillus and Bacteroidetes were higher in the GDM-I group than in the non-GDM and GDM-D groups. After treatment, gut microbiota composition showed no difference between non-GDM and GDM-I groups. Interestingly, a higher Firmicutes/Bacteroidetes (F/B) ratio was displayed in GDM-D mothers at posttreatment, and this was also observed in both meconium and first feces of GDM-D newborns. ConclusionInsulin therapy changed maternal gut microbiota composition, which could be transferable to the mothers’ newborns.

Gut Dysbiosis Has the Potential to Reduce the Sexual Attractiveness of Mouse Female.

Increasing evidence has shown that the gut microbiome has significant effects on mate preferences of insects; however, whether gut microbiota composition affects sexual attractiveness and mate preference in mammals remains largely unknown. Here, we showed that antibiotic treatment significantly restructured the gut microbiota composition of both mouse males and females. Males, regardless of antibiotic treatment, exhibited a higher propensity to interact with the control females than the antibiotic-treated females. The data clearly showed that gut microbiota dysbiosis reduced the sexual attractiveness of females to males, implying that commensal gut microbiota influences female attractiveness to males. The reduced sexual attractiveness of the antibiotic-treated females may be beneficial to discriminating males by avoiding disorders of immunity and sociability in offspring that acquire maternal gut microbiota via vertical transmission. We suggest further work should be oriented to increase our understanding of the interactions between gut microbiota dysbiosis, sexual selection, and mate choice of wild animals at the population level.

Effects of the maternal gut microbiome and gut-placental axis on melatonin efficacy in alleviating cadmium-induced fetal growth restriction

Cadmium (Cd) is a major environmental stressor that induces fetal growth restriction (FGR). Also, changes in gut microbiome diversity-which can be modulated positively by melatonin (Mel) have implications on fetal development and placental functions. Therefore, this study aimed to explore whether the role of Mel in counteracting the Cd-induced FGR by regulating placental barrier injury, endoplasmic reticulum stress (ERS) and mitophagy in pregnant mice is mediated-in part- via the gut microbiota modulations. Pregnant mice were intraperitoneally injected with CdCl2 (5 mg/kg) and Mel (5 mg/kg) once daily, respectively, at the same time from gestational day (GD) 8 to GD18, and then the maternal colon and placental tissues were collected for detection. To investigate the inner relationship between intestinal flora and the protection of Mel on FGR caused by Cd, gut microbiota transplantation (GMT) was carried out from GD0 to GD18 after the removal of intestinal microbiota by antibiotics. Results indicated that Mel relieved barrier injury, ERS and mitophagy in the placenta, and reversed the maternal gut microbiota dysbiosis. The GMT approach suggested a role of intestinal microbiota in placental barrier injury, ERS and mitophagy induced by Cd. Overall, the results highlighted that the intestinal microbiota and gut-placental axis play a central role in the protective effect of Mel against Cd-induced FGR.

Dynamics of the infant gut microbiota in the first 18 months of life: the impact of maternal HIV infection and breastfeeding

BackgroundAccess to antiretroviral therapy (ART) during pregnancy and breastfeeding for mothers with HIV has resulted in fewer children acquiring HIV peri- and postnatally, resulting in an increase in the number of children who are exposed to the virus but are not infected (HEU). HEU infants have an increased likelihood of childhood infections and adverse growth outcomes, as well as increased mortality compared to their HIV-unexposed (HUU) peers. We explored potential differences in the gut microbiota in a cohort of 272 Nigerian infants born to HIV-positive and negative mothers in this study during the first 18 months of life.ResultsThe taxonomic composition of the maternal vaginal and gut microbiota showed no significant differences based on HIV status, and the composition of the infant gut microbiota at birth was similar between HUU and HEU. Longitudinal taxonomic composition of the infant gut microbiota and weight-for-age z-scores (WAZ) differed depending on access to breast milk. HEU infants displayed overall lower WAZ than HUU infants at all time points. We observed a significantly lower relative abundance of Bifidobacterium in HEU infants at 6 months postpartum. Breast milk composition also differed by time point and HIV infection status. The antiretroviral therapy drugs, lamivudine and nevirapine, as well as kynurenine, were significantly more abundant in the breast milk of mothers with HIV. Levels of tiglyl carnitine (C5) were significantly lower in the breast milk of mothers without HIV. ART drugs in the breast milk of mothers with HIV were associated with a lower relative abundance of Bifidobacterium longum.ConclusionsMaternal HIV infection was associated with adverse growth outcomes of HEU infants in this study, and these differences persist from birth through at least 18 months, which is a critical window for the development of the immune and central nervous systems. We observed that the relative abundance of Bifidobacterium spp. was significantly lower in the gut microbiota of all HEU infants over the first 6 months postpartum, even if HEU infants were receiving breast milk. Breastfeeding was of benefit in our HEU infant cohort in the first weeks postpartum; however, ART drug metabolites in breast milk were associated with a lower abundance of Bifidobacterium.7evEDGTh3wF9QF2c-7o-e3Video abstract

Probiotics ameliorates LPS induced neuroinflammation injury on Aβ 1-42, APP, γ-β secretase and BDNF levels in maternal gut microbiota and fetal neurodevelopment processes.

The gut microbiota influences brain development and functioning through the gut-brain axis. This is first study regulate maternal gut microbiota and fetal neurodevelopment processes by using probiotics such as Bifidobacterium bifidum (BIF) and Lactobacillus salivarius (LAC) in the prenatal period. In this study, Wistar Albino female rats were divided into five groups; Control, lipopolysaccharide (LPS, 100µg/kg), LPS + LAC, LPS + BIF and LPS + LAC + BIF (4 × 109mlCFU). Maternal rats were given probiotics for 21days. Inflammation was induced by lipopolysaccharide (LPS), on the 17th day of pregnancy. After birth, the brain tissues of the maternal and neonatal rats were removed and their blood was collected. Fecal calprotectin levels of pregnant rats were measured as an important biomarker in determining intestinal flora disruption. Calprotectin levels were high in LPS group (p < 0.05). Aβ 1-42, APP, γ secretase and β- secretase levels were higher in both maternal and neonatal LPS groups (p < 0.05). These levels were statistically decreased in the probiotic groups compared to the LPS group, as demonstrated in both biochemical and histological analyzes (p < 0.05). While BDNF mRNA expression decreased in LPS groups, APP level increased in the same group. The difference between groups in mRNA expressions in the neonatal brain tissues was similar to maternal brain tissues. What's more, BDNF/actin and APP/actin rates were proven by western blot and the damage caused by neuroinflammation in the brain tissue and the preservation of the intestinal microbiota were visualized histopathologically on the morphological structures in all groups. It will shed light on new therapeutic strategies for the impact of the use of probiotics on the neurodevelopmental processes of the neonatal against LPS-induced inflammatory responses and impaired gut microbiota in the prenatal period.

The Maternal-Fetal Gut Microbiota Axis: Physiological Changes, Dietary Influence, and Modulation Possibilities.

The prenatal period and the first years of life have a significant impact on the health issues and life quality of an individual. The appropriate development of the immune system and the central nervous system are thought to be major critical determining events. In parallel to these, establishing an early intestinal microbiota community is another important factor for future well-being interfering with prenatal and postnatal developmental processes. This review aims at summarizing the main characteristics of maternal gut microbiota and its possible transmission to the offspring, thereby affecting fetal and/or neonatal development and health. Since maternal dietary factors are potential modulators of the maternal–fetal microbiota axis, we will outline current knowledge on the impact of certain diets, nutritional factors, and nutritional modulators during pregnancy on offspring’s microbiota and health.

Food allergies, intestinal microbiota and probiotics

There are many studies devoted to the study of the intestinal microbiota. They prove the leading role of microorganisms in the formation of the immune response of the host. Intestinal microbiota contributes to the switch of preferential differentiation of Th-lymphocytes from Th2-type, typical for newborns, to the formation of Tr-cells (regulatory) with a corresponding increase in the formation of TGF-β and IL-10. Consequently, immunological tolerance is formed under the influence of the intestinal microbiota. This process occurs in the first months of life and has a long-term effect, setting the features of the body’s immune response to external infectious and food antigens, which determines the predisposition to the development of food allergies later in life. This article describes the factors that influence the colonization of the baby’s gut. Maternal gut microbiota, maternal health, mode of delivery (natural childbirth or cesarean section), type of feeding (breastfeeding or formula feeding) - all these factors affect the colonization of the gut and the formation of an immune response. In addition, lactobacilli and bifidobacteria play a critical role in the formation of immunological tolerance. Probiotics can modulate the immune response similar to the intestinal microbiota. Lactobacillus and bifidobacterium infant strains are optimal. Clinical studies have proven the effectiveness of perinatal and early administration of probiotics for the prevention of food allergies. A balanced combination of Lactobacillus rhamnosus and Bifidobacterium longum is a symbiosis of bacteria that enhances the effectiveness of each other, which promotes the optimal establishment of the intestinal microbiocenosis from birth and is the prevention of both infectious diseases and food allergies. A combination probiotic containing both Lactobacillus rhamnosus and Bifidobacterium longum seems to be the optimal choice.

The intestine and the microbiota in maternal glucose homeostasis during pregnancy.

It is now well established that, beyond its role in nutrient processing and absorption, the intestine and its accompanying gut microbiome constitute a major site of immunological and endocrine regulation that mediates whole-body metabolism. Despite the growing field of host-microbe research, few studies explore what mechanisms govern this relationship in the context of pregnancy. During pregnancy, significant maternal metabolic adaptations are made to accommodate the additional energy demands of the developing fetus and to prevent adverse pregnancy outcomes. Recent data suggest that the maternal gut microbiota may play a role in these adaptations, but changes to maternal gut physiology and the underlying intestinal mechanisms remain unclear. In this review, we discuss selective aspects of intestinal physiology including the role of the incretin hormone, glucagon-like peptide 1 (GLP-1), and the role of the maternal gut microbiome in the maternal metabolic adaptations to pregnancy. Specifically, we discuss how bacterial components and metabolites could mediate the effects of the microbiota on host physiology, including nutrient absorption and GLP-1 secretion and action, and whether these mechanisms may change maternal insulin sensitivity and secretion during pregnancy. Finally, we discuss how these pathways could be altered in disease states during pregnancy including maternal obesity and diabetes.

Maternal sleep deprivation induces gut microbial dysbiosis and neuroinflammation in offspring rats.

Maternal sleep deprivation (MSD) is a global public health problem that affects the physical and mental development of pregnant women and their newborns. The latest research suggests that sleep deprivation (SD) disrupts the gut microbiota, leading to neuroinflammation and psychological disturbances. However, it is unclear whether MSD affects the establishment of gut microbiota and neuroinflammation in the newborns. In the present study, MSD was performed on pregnant Sprague-Dawley rats in the third trimester of pregnancy (gestational days 15–21), after which intestinal contents and brain tissues were collected from offspring at different postnatal days (P1, P7, P14, and P56). Based on microbial profiling, microbial diversity and richness increased in pregnant rats subjected to MSD, as reflected by the significant increase in the phylum Firmicutes. In addition, microbial dysbiosis marked by abundant Firmicutes bacteria was observed in the MSD offspring. Furthermore, quantitative real-time polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA) showed that the expression levels of proinflammatory cytokines interleukin 1β (IL-1β) and tumor necrosis factor α (TNF-α) were significantly higher in the MSD offspring at adulthood (P56) than in the control group. Through Spearman correlation analysis, IL-1β and TNF-α were also shown to be positively correlated with Ruminococcus_1 and Ruminococcaceae_UCG-005 at P56, which may determine the microbiota-host interactions in MSD-related neuroinflammation. Collectively, these results indicate that MSD changes maternal gut microbiota and affects the establishment of neonatal gut microbiota, leading to neuroinflammation in MSD offspring. Therefore, understanding the role of gut microbiota during physiological development may provide potential interventions for cognitive dysfunction in MSD-impacted offspring.

Comparison of Gut Microbiota and Metabolic Status of Sows With Different Litter Sizes During Pregnancy.

The experiment was conducted to compare the differences of gut microbiota and metabolic status of sows with different litter sizes on days 30 and 110 of gestation, and uncover the relationship between the composition of maternal gut microbiota during gestation and sow reproductive performance. Twenty-six Large White × Landrace crossbred multiparous sows (2nd parity) with similar back fat thickness and body weight were assigned to two groups [high-reproductive performance group (HP group) and low-reproductive performance group (LP group)] according to their litter sizes and fed a common gestation diet. Results showed that compared with LP sows, HP sows had significantly lower plasma levels of triglyceride (TG) on gestation d 30 (P < 0.05), but had significantly higher plasma levels of TG, non-esterified fatty acid, tumor necrosis factor-α, and immunoglobulin M on gestation d 110 (P < 0.05). Consistently, HP sows revealed increased alpha diversity and butyrate-producing genera, as well as fecal butyrate concentration, on gestation d 30; HP sows showed significantly different microbiota community structure with LP sows (P < 0.05) and had markedly higher abundance of Firmicutes (genera Christensenellaceae_R-7_group and Terrisporobacter) which were positively related with litter size on gestation d 110 than LP sows (P < 0.05). In addition, plasma biochemical parameters, plasma cytokines, and fecal microbiota shifted dramatically from gestation d 30 to d 110. Therefore, our findings demonstrated that microbial abundances and community structures differed significantly between sows with different litter sizes and gestation stages, which was associated with changes in plasma biochemical parameters, inflammatory factors, and immunoglobulin. Moreover, these findings revealed that there was a significant correlation between litter size and gut microbiota of sows, and provided a microbial perspective to improve sow reproductive performance in pig production.

Maternal Obesity Related to High Fat Diet Induces Placenta Remodeling and Gut Microbiome Shaping That Are Responsible for Fetal Liver Lipid Dysmetabolism.

Background: Maternal obesity in utero may affect fetal development and cause metabolic problems during childhood and even adulthood. Diet-induced maternal obesity can impair gut barrier integrity and change the gut microbiome, which may contribute to adverse placental adaptations and increase the obesity risk in offspring. However, the mechanism through which maternal obesity causes offspring metabolic disorder must be identified.Methods: Eight-week-old female rats received a control diet or high-fat (HF) diet for 11 weeks before conception and during gestation. The placentas were collected on gestational day 21 before offspring delivery. Placental tissues, gut microbiome, and short-chain fatty acids of dams and fetal liver tissues were studied.Results: Maternal HF diet and obesity altered the placental structure and metabolism-related transcriptome and decreased G protein–coupled receptor 43 expression. HF diet and obesity also changed the gut microbiome composition and serum propionate level of dams. The fetal liver exhibited steatosis, enhanced oxidative stress, and increased expression of acetyl-CoA carboxylase 1 and lipoprotein lipase with changes in maternal HF diet and obesity.Conclusions: Maternal HF diet and obesity shape gut microbiota and remodel the placenta of dams, resulting in lipid dysmetabolism of the fetal liver, which may ultimately contribute to the programming of offspring obesity.

Fecal Bacterial Communities Differ by Lactation Status in Postpartum Women and Their Infants.

Previous research examined effects of human milk on the infant gut microbiota, but little attention has been given to the microbiota of lactating women. To determine associations between exclusive human milk feeding and gut microbiota characteristics in mothers and infants at 6-weeks postpartum. A sample of mother-infant dyads (N = 24) provided fecal samples and questionnaire responses at 6-weeks postpartum as part of the Pregnancy, EAting & POstpartum Diapers study. Deoxyribonucleic acid was extracted from stool samples, followed by (V4) 16S ribosomal ribonucleic acid gene amplicon sequencing. Alpha and beta diversity, in addition to taxa differences, were compared by human milk exposure status, exclusive versus non-exclusive. A subset of dyads (those exclusively fed human milk; n = 14) was analyzed for shared bifidobacterial species using polymerase chain reaction. Alpha diversity was significantly lower in exclusively human milk-fed infants. Maternal lactation status (exclusive vs. partial) and Shannon diversity were associated in univariate analysis but were no longer associated in multivariable regression including body mass index category in the model. Beta diversity (Sorensen dissimilarity) of fecal samples from women and infants was significantly associated with human milk feeding. Of six infants with Bifidobacterium longum subspecies longum in their fecal samples, all their mothers shared the same species. Maternal gut microbiotas differ by lactation status, a relationship potentially confounded by body mass index category. Further research is needed to identify whether lactation directly influences the maternal gut microbiota, which may be another mechanism by which lactation influences health.

Maternal gut bacteria drive intestinal inflammation in offspring with neurodevelopmental disorders by altering the chromatin landscape of CD4+ T cells

Children with autism spectrum disorders often display dysregulated immune responses and related gastrointestinal symptoms. However, the underlying mechanisms leading to the development of both phenotypes have not been elucidated. Here, we show that mouse offspring exhibiting autism-like phenotypes due to prenatal exposure to maternal inflammation were more susceptible to developing intestinal inflammation following challenges later in life. In contrast to its prenatal role in neurodevelopmental phenotypes, interleukin-17A (IL-17A) generated immune-primed phenotypes in offspring through changes in the maternal gut microbiota that led to postnatal alterations in the chromatin landscape of naive CD4+ Tcells. The transfer of stool samples from pregnant mice with enhanced IL-17A responses into germ-free dams produced immune-primed phenotypes in offspring. Our study provides mechanistic insights into why children exposed to heightened inflammation in the womb might have an increased risk of developing inflammatory diseases in addition to neurodevelopmental disorders.

Composition of the microbial communities at different body sites in women with preterm birth and their newborns

ObjectiveIn this study, we aimed to examine the changes in the composition of vaginal and gut microbiota during the third trimester of pregnancy among women who delivered preterm. To further understand the relationship of these changes to preterm birth, we analyzed the microecology of vaginal and gut microbiota in mothers, as well as oral and gut microbiota in their newborns, and then compared the microecological characteristics of the microbiome at different body sites between the mothers and their newborns, as well as between the mothers and between the newborns from different groups. MethodsIn total, 26 women who delivered at Zhujiang Hospital, Southern Medical University (China) from July 2020 to January 2021 were categorized into the preterm and term groups. A blank swab and laboratory air and water samples were collected as part of the control group. We collected maternal vaginal and rectal samples, as well as neonatal oral and rectal samples. Total DNA from different parts of the swabs was extracted and sequenced using the 16s rRNA technique. Then, the data was analyzed using bioinformatics and statistical analysis. ResultsThe abundance and alpha diversity of vaginal microbiota in the preterm group was found to be higher, but the difference was not statistically significant. There were significant differences in beta diversity of vaginal microbiota between the two groups (p ​< ​0.05). The levels of Rothia and Gemella in the gut microbiota of women who had delivered preterm were significantly lower (p ​< ​0.05). The alpha diversity of gut microbiota and neonatal oral and gut microbiota in women who had delivered preterm was lower. No significant differences were observed in alpha and beta diversity between the two groups in maternal gut microbiota and neonatal oral and gut microbiota. In the newborns in both groups, some species of oral microbiota were consistent with their mother's vaginal microbiota, and some species of gut microbiota in the newborns in both groups were consistent with their mother's gut microbiota. ConclusionsVaginal and gut microbiota in women who had given birth preterm were noticeably different from the vaginal and gut microbiota of women who had delivered at term, and it was probably related to preterm birth. Oral and gut microbiotas of preterm newborns were also noted to be different from that of the term newborns. It suggests that the changes in the microbiome of the newborns could be related to preterm birth. Some part of the newborns’ microbiota probably originates in the uterus.

C-section birth increases offspring obesity risk dependent on maternal diet and obesity status in rats.

The gut microbiota is a complex ecosystem that shapes host metabolism, especially in early life. Maternal vaginal and gut microbiota is vertically transmitted to offspring during natural birth. Offspring born by cesarean section (CS) do not receive these bacteria and exhibit higher obesity risk later in life. The objective of this study was to examine differences in obesity risk between offspring born naturally (NB) or by CS to lean/obese dams. Lean and obese rat dams gave birth to offspring naturally or by CS. Offspring obesity risk was analyzed via body weight/composition, food intake, sucrose preference, gut microbiota, and gene expression in gut and brain tissues. Obese (O)+CS offspring showed greater weight gain and caloric intake but a reduction in hypothalamic agouti related neuropeptide, neuropeptide Y, and interleukin 1β expression compared with O+NB offspring. Lean (L)+CS offspring had higher serum corticosterone concentration and reduced liver peroxisome proliferator-activated receptor γ expression compared with L+NB. O+CS offspring had long-term alterations to gut microbiota, including increased relative abundance of Faecalibaculum and reduced Muribaculaceae. Overall, CS alters obesity risk differentially based on maternal obesity status. Further studies looking at the risks of obesity associated with CS are needed, with special attention paid to maternal obesity status and gut microbiota.

Maternal Gut Dysbiosis Alters Offspring Microbiota and Social Interactions.

Increasing application of antibiotics changes the gut microbiota composition, leading to dysbiosis of the gut microbiota. Although growing evidence suggests the potential role of gut dysbiosis as the cause of neurodevelopmental disorders and behavioral defects, a broad gap of knowledge remains to be narrowed to better understand the exact mechanisms by which maternal gut dysbiosis alters microbiota development and social interactions of offspring. Here, we showed that maternal gut dysbiosis during gestation is a critical determinant of gut microbiota and social interactions off mouse offspring. Gut microbiota of 2-week-old offspring showed significant changes in response to maternal antibiotic treatment. We even detected distinct effects of maternal oral antibiotics on gut microbiota of 14-week-old offspring. Compared to controls, offspring born to antibiotics-treated mothers displayed reduction in sociability and preference for social novelty, suggesting that the altered offspring social behavior was closely linked to dysbiosis of maternal gut microbiota. Our study opens the possibility to better understand the mechanism of how maternal gut microbiota vertically impairs social interactions of offspring in animal models, providing support to the maternal gut microbiota as a potential mediator between offspring microbiota and behaviors.

Association between Gut Microbiota and Development of Gestational Diabetes Mellitus.

Background: It is well known that women with gestational diabetes mellitus (GDM) have gut dysbiosis. However, the dynamic alterations of gut microbiota in GDM are unclear. Additionally, the effects of maternal gut microbiota on the gut microbiota of their newborns remains controversial. The primary objective of this study is to determine the association between types and amounts of gut microbiota and development of gestational diabetes mellitus (GDM). Methods: Eighty-eight pregnant women, including 39 non-GDM and 49 GDM, and their 88 offspring were enrolled. Maternal feces were collected at the time of GDM diagnosis (24–28 weeks of gestation) and at before delivery (≥37 weeks of gestation). Meconium and the first feces of their newborns were also obtained. Results: from quantitative polymerase chain reaction (qPCR) showed that maternal Lactobacillales was decreased from baseline to the time before delivery in both non-GDM and GDM. Firmicutes/Bacteroidetes (F/B) ratio at before delivery was higher in the GDM group. However, there was no difference of neonatal gut microbiota between groups. Conclusions: Although we found only few gut microbiota that demonstrated the difference between GDM and non-GDM, gut microbiota may play a more important role in the development of severer GDM. Therefore, a further study comparing the gut microbiota composition among non-GDM, GDM with diet modification only, GDM with insulin therapy, GDM with successful treatment, and GDM with failure of treatment is needed.

An Insight into Probiotics Bio-Route: Translocation from the Mother’s Gut to the Mammary Gland

Human breast milk (HBM) is unique in its composition as it is adapted to fulfil the newborns’ nutritional requirement and helps in improving the health of newborns. Besides various nutrients, the human milk also contains diverse group of microbiotas. The human milk microbiota has a remarkable impact on the growth and development of a newborn. Additionally, the human milk microbiota enhances the colonization of microbes in the gut of infants. Debates about the origin of HBM microbial flora remain premature and contradictory in some cases. Recent data suggest that the maternal gut microbiota has a major impact on microbial composition, areolar skin, and from the infant’s oral cavity. The current review investigates the possible route of microbial transfer from the maternal gut to mammary gland and suggests that it might occur through the entero-mammary pathway. It involves precise selection of probiotic microorganisms from the gut, as the human gut hosts trillions of microorganisms involved in gut homeostasis and other metabolic pathways. Gastrointestinal lymphatic vessels, macrophages, and dendritic cells are shown to play a significant role in the microbial transmission. Furthermore, the role of microbial factors in the development of neonatal immunity and translocation of secretory IgA (SIgA) cells from the intestinal lumen to GALT and finally to mammary glands via entero-mammary link are discussed.

Spontaneous preterm delivery is reflected in both early neonatal and maternal gut microbiota

BackgroundAberrant gut microbiota composition in preterm neonates is linked to adverse health consequences. Little is known about the impact of perinatal factors or maternal gut microbiota on initial preterm gut colonization.MethodsFecal samples were collected from 55 preterm neonates (<35 gestational weeks), 51 mothers, and 25 full-term neonates during the first 3–4 postpartum days. Gut microbiota composition was assessed using 16S ribosomal RNA gene sequencing.ResultsPreterm neonates exhibited significantly lower gut microbiota alpha diversity and distinct beta diversity clustering compared to term neonates. Spontaneous preterm birth was associated with distinct initial gut microbiota beta diversity as compared to iatrogenic delivery. Gestational age or delivery mode had no impact on the preterm gut microbiota composition. The cause of preterm delivery was also reflected in the maternal gut microbiota composition. The contribution of maternal gut microbiota to initial preterm gut colonization was more pronounced after spontaneous delivery than iatrogenic delivery and not dependent on delivery mode.ConclusionsThe initial preterm gut microbiota is distinct from term microbiota. Spontaneous preterm birth is reflected in the early neonatal and maternal gut microbiota. Transmission of gut microbes from mother to neonate is determined by spontaneous preterm delivery, but not by mode of birth.ImpactThe initial gut microbiota in preterm neonates is distinct from those born full term. Spontaneous preterm birth is associated with changes in the gut microbiota composition of both preterm neonates and their mothers. The contribution of the maternal gut microbiota to initial neonatal gut colonization was more pronounced after spontaneous preterm delivery as compared to iatrogenic preterm delivery and not dependent on delivery mode.Our study provides new evidence regarding the early gut colonization patterns in preterm infants.Altered preterm gut microbiota has been linked to adverse health consequences and may provide a target for early intervention.

Impacts of PBDE-47 exposure before, during and after pregnancy on the maternal gut microbiome and its association with host metabolism

Maternal gut microbiota play an important role in the modulation of offspring disease susceptibility and gut microbiota dysbiosis has been proposed as a mechanism through which toxic environmental chemicals exert their adverse impacts on health. The brominated flame retardants polybrominated diphenyl ethers (PBDEs) are developmental toxicants and induce dysbiotic gut microbiota in offspring. Yet, whether and how PBDEs impact the maternal gut microbiota remain unclear. Here, we sought to investigate the effect of 2,2′,4,4′-tetrabromodiphenyl ether (PBDE-47) exposure from preconception through lactation cessation on maternal gut microbiota and its link to host serum metabolic consequences. Female Sprague-Dawley rats were daily exposed to 10 mg/kg PBDE-47 via oral gavage from ten days before conception until offspring were weaned on postnatal day 21, then maternal fecal and blood samples were collected for microbiome and metabolome analyses by using 16S ribosomal RNA gene sequencing and gas chromatography-mass spectrometry, respectively. Maternal exposure to PBDE-47 showed a distinct profile in gut microbiota compared to control dams, as evidenced by increased Actinobacteria phylum and genera Blautia, Gemella and Phascolarctobacterium, and decreased genera AF12 and Oscillospira. Additionally, global metabolomics analysis identified 26 differential serum metabolites to distinguish PBDE-47 from controls, which were mainly involved in amino acid, lipid, carbohydrate and energy metabolism, further confirmed by pathway analysis. Importantly, the differential serum metabolites are closely correlated with the disturbed gut microbiota in response to PBDE-47. Collectively, our results suggest that maternal gut microbial dysbiosis may serve as a potential mechanism underlying PBDE-47-elicited health hazards to mothers or even offspring.