Colonization Of Gut Microbiota Research Articles

A mixture of quebracho and chestnut tannins drives butyrate-producing bacteria populations shift in the gut microbiota of weaned piglets.

Weaning is a critical period for piglets, in which unbalanced gut microbiota and/or pathogen colonisation can contribute to diseases that interfere with animal performance. Tannins are natural compounds that could be used as functional ingredients to improve gut health in pig farming thanks to their antibacterial, antioxidant, and antidiarrhoeal properties. In this study, a mixture of quebracho and chestnut tannins (1.25%) was evaluated for its efficacy in reducing the negative weaning effects on piglet growth. Microbiota composition was assessed by Illumina MiSeq 16S rRNA gene sequencing of DNA extracted from stools at the end of the trial. Sequence analysis revealed an increase in the genera Shuttleworthia, Pseudobutyrivibrio, Peptococcus, Anaerostipes, and Solobacterium in the tannin-supplemented group. Conversely, this dietary intervention reduced the abundance of the genera Syntrophococcus, Atopobium, Mitsuokella, Sharpea, and Prevotella. The populations of butyrate-producing bacteria were modulated by tannin, and higher butyrate concentrations in stools were detected in the tannin-fed pigs. Co-occurrence analysis revealed that the operational taxonomic units (OTUs) belonging to the families Veillonellaceae, Lachnospiraceae, and Coriobacteriaceae occupied the central part of the network in both the control and the tannin-fed animals. Instead, in the tannin group, the OTUs belonging to the families Acidaminococcaceae, Alcaligenaceae, and Spirochaetaceae characterised its network, whereas Family XIII Incertae Sedis occupied a more central position than in the control group. Conversely, the presence of Desulfovibrionaceae characterised the network of the control group, and this family was not present in the network of the tannin group. Moreover, the prediction of metabolic pathways revealed that the gut microbiome of the tannin group possessed an enhanced potential for carbohydrate transport and metabolism, as well as a lower abundance of pathways related to cell wall/membrane/envelope biogenesis and inorganic ion transport. In conclusion, the tested tannins seem to modulate the gut microbiota, favouring groups of butyrate-producing bacteria.

Impact of Maternal Nutritional Supplementation during Pregnancy and Lactation on the Infant Gut or Breastmilk Microbiota: A Systematic Review.

Recent evidence indicates that maternal dietary intake, including dietary supplements, during pregnancy and lactation may alter the infant gut or breastmilk microbiota, with implications for health outcomes in both the mother and infant. To review the effects of maternal nutritional supplementation during pregnancy and lactation on the infant gut or breastmilk microbiota a systematic literature search was conducted. A total of 967 studies published until February 2020 were found, 31 were eligible and 29 randomized control trials were included in the qualitative synthesis. There were 23 studies that investigated the effects of probiotic supplementation, with the remaining studies investigating vitamin D, prebiotics or lipid-based nutrient supplements (LNS). The effects of maternal nutritional supplementation on the infant gut microbiota or breastmilk microbiota were examined in 21 and 12 studies, respectively. Maternal probiotic supplementation during pregnancy and lactation generally resulted in the probiotic colonization of the infant gut microbiota, and although most studies also reported alterations in the infant gut bacterial loads, there was limited evidence of effects on bacterial diversity. The data available show that maternal probiotic supplementation during pregnancy or lactation results in probiotic colonization of the breastmilk microbiota. There were no observed effects between probiotic supplementation and breastmilk bacterial counts of healthy women, however, administration of Lactobacillus probiotic to nursing women affected by mastitis was associated with significant reductions in breastmilk Staphylococcal loads. Maternal LNS supplementation during pregnancy and lactation increased bacterial diversity in the infant gut, whilst vitamin D and prebiotic supplementation did not alter either infant gut bacterial diversity or counts. Heterogeneity in study design precludes any firm conclusions on the effects of maternal nutritional supplementation during pregnancy and lactation on the infant gut or breastmilk microbiota, warranting further research.

Unravelling the potential of gut microbiota in sustaining brain health and their current prospective towards development of neurotherapeutics.

Increasing incidences of neurological disorders, such as Parkinson's disease (PD), multiple sclerosis (MS), Alzheimer's disease (AD) and amyotrophic lateral sclerosis (ALS) are being reported, but an insight into their pathology remains elusive. Findings have suggested that gut microbiota play a major role in regulating brain functions through the gut-brain axis. A unique bidirectional communication between gut microbiota and maintenance of brain health could play a pivotal role in regulating incidences of neurodegenerative diseases. Contrarily, the present life style with changing food habits and disturbed circadian rhythm may contribute to gut homeostatic imbalance and dysbiosis leading to progression of several neurological disorders. Therefore, dysbiosis, as a primary factor behind intestinal disorders, may also augment inflammation, intestinal and blood-brain barrier permeability through microbiota-gut-brain axis. This review primarily focuses on the gut-brain axis functions, specific gut microbial population, metabolites produced by gut microbiota, their role in regulating various metabolic processes and role of gut microbiota towards development of neurodegenerative diseases. However, several studies have reported a decrease in abundance of a specific gut microbial population and a corresponding increase in other microbial family, with few findings revealing some contradictions. Reports also showed that colonization of gut microbiota isolated from patients suffering from neurodegenerative disease leads to the development of enhance pathological outcomes in animal models. Hence, a systematic understanding of the dominant role of specific gut microbiome towards development of different neurodegenerative diseases could possibly provide novel insight into the use of probiotics and microbial transplantation as a substitute approach for treating/preventing such health maladies.

Gut microbiota diversity but not composition is related to saliva cortisol stress response at the age of 2.5 months

Human brain and intestinal microbes reportedly maintain a constant bidirectional connection through diverse neural, endocrine, immune, and metabolic pathways. Increasing evidence indicates that this communication system, referred to as microbiota-gut-brain axis, enables the gut microbes to influence several aspects of brain function and behavior, including hypothalamic-pituitary-adrenal (HPA) axis stress responses, and on the other hand, stress can affect gut microbiota. However, the role of gut microbiota in the HPA axis functioning in humans remains to be specified especially in early life. This study aimed at identifying the potential link between the cortisol stress response and the gut microbiota at the age of 2.5 months. Fecal microbiota profiles were acquired by 16S rRNA gene sequencing, while salivary cortisol responses after an exposure to a mild acute stressor represented the HPA axis reactivity. We observed that a blunted cortisol stress response was weakly associated with a diverse gut microbiota diversity at the age of 2.5 months. Gut microbiota composition was not associated with cortisol stress responsiveness, but rather with covariates, i.e. factors that influence gut microbiota composition and colonization. LAY SUMMARY This exploratory study aimed at identifying possible links between cortisol stress responses and fecal microbiota composition in early infancy. In a well-characterized study population of 2.5-month-old infants, we observed that an attenuated cortisol stress responsiveness after a mild stressor was weakly associated with a diverse fecal microbiota. Our results suggest that the gut microbiota composition is associated with environmental factors, such as delivery mode and number of siblings, rather than with cortisol stress responsiveness, in this age group.

Do Probiotics During In-Hospital Antibiotic Treatment Prevent Colonization of Gut Microbiota With Multi-Drug-Resistant Bacteria? A Randomized Placebo-Controlled Trial Comparing Saccharomyces to a Mixture of Lactobacillus, Bifidobacterium, and Saccharomyces.

Objective: Most infections with Enterobacteriaceae producing AmpC β-lactamase (AmpC)-, extended-spectrum β-lactamase (ESBL)-, and carbapenemase-producing bacteria, vancomycin-resistant Enterococcus as well as naturally resistant non-fermenting bacteria such as Pseudomonas aeruginosa, are related to a prior colonization of the gut microbiota. The objective of this study was to determine whether treatment with probiotics during an antibiotic treatment could prevent the colonization of the gut microbiota with multi-drug resistant bacteria.Method: In total, 120 patients treated for 10 days with amoxicillin-clavulanate antibiotics were included in a randomized, placebo-controlled, double-blinded trial, comparing the effects of a 30 days treatment with placebo Saccharomyces boulardii CNCM I-745® and a probiotic mixture containing Saccharomyces boulardii, Lactobacillus acidophilus NCFM, Lactobacillus paracasei Lpc-37, Bifidobacterium lactis Bl-04, and Bifidobacterium lactis Bi-07 (Bactiol duo®). Study treatment was initiated within 48 h of the antibiotic being initiated. Most of the patients included were elderly with a mean age of 78 years old with multiple comorbidities. Stools were collected at the time of inclusion in the trial, at the end of the antibiotic treatment, and the end of the study treatment. These were cultured on selective antibiotic media.Results: Treatment with the probiotic mixture led to a significant decline in colonization with Pseudomonas after antibiotic treatment from 25 to 8.3% (p = 0.041). Colonization with AmpC-producing enterobacteria was transiently increased after the antibiotic treatment (p = 0.027) and declined after the probiotic intervention (p= 0.041). No significant changes were observed in the placebo and Saccharomyces groups. Up to 2 years after the trial, no infection with ESBL-producing bacteria was observed in the probiotic mixture group.Conclusion: The association of Saccharomyces boulardii with specific strains of Lactobacillus and Bifidobacterium influences antibiotic treatment by counteracting the colonization of the colon microbiota with antibiotic-resistant pathogens.

Neurodevelopmental Outcomes and Gut Bifidobacteria in Term Infants Fed an Infant Formula Containing High sn-2 Palmitate: A Cluster Randomized Clinical Trial.

A few studies suggested high stereo-specifically numbered (sn)-2 palmitate in a formula might favor the gut Bifidobacteria of infants. The initial colonization and subsequent development of gut microbiota in early life might be associated with development and later life functions of the central nervous system via the microbiota–gut–brain axis, such as children with autism. This study aims to assess the hypothesized effect of increasing the amount of palmitic acid esterified in the sn-2 position in infant formula on neurodevelopment in healthy full-term infants and to explore the association of this effect with the altered gut Bifidobacteria. One hundred and ninety-nine infants were enrolled in this cluster randomized clinical trial: 66 breast-fed (BF group) and 133 formula-fed infants who were clustered and randomly assigned to receive formula containing high sn-2 palmitate (sn-2 group, n = 66) or low sn-2 palmitate (control group, n = 67), where 46.3% and 10.3% of the palmitic acid (PA) was sn-2-palmitate, respectively. Infants’ neurodevelopmental outcomes were measured by the Ages and Stages Questionnaire, third edition (ASQ-3). Stool samples were collected for the analysis of Bifidobacteria (Trial registration number: ChiCTR1800014479). At week 16, the risk of scoring close to the threshold for fine motor skills (reference: scoring above the typical development threshold) was significantly lower in the sn-2 group than the control group after adjustment for the maternal education level (p = 0.036) but did not differ significantly versus the BF group (p = 0.513). At week 16 and week 24, the sn-2 group (week 16: 15.7% and week 24: 15.6%) had a significantly higher relative abundance of fecal Bifidobacteria than the control group (week 16: 6.6%, p = 0.001 and week 24:11.2%, p = 0.028) and did not differ from the BF group (week 16: 14.4%, p = 0.674 and week 24: 14.9%, p = 0.749). At week 16, a higher relative abundance of Bifidobacteria was associated with the decreased odds of only one domain scoring close to the threshold in the formula-fed infants group (odds ratio (OR), 95% confidence interval (CI): 0.947 (0.901–0.996)). Elevating the sn-2 palmitate level in the formula improved infants’ development of fine motor skills, and the beneficial effects of high sn-2 palmitate on infant neurodevelopment was associated with the increased gut Bifidobacteria level.

Characterization of rat and mouse acidic milk oligosaccharides based on hydrophilic interaction chromatography coupled with electrospray tandem mass spectrometry

Oligosaccharides are one of the most important components in mammalian milk. Milk oligosaccharides can promote colonization of gut microbiota and protect newborns from infections. The diversity and structures of MOs differ among mammalian species. MOs in human and farm animals have been well-documented. However, the knowledge on MOs in rat and mouse have been very limited even though they are the most-widely used models for studies of human physiology and disease. Herein, we use a high-sensitivity online solid-phase extraction and HILIC coupled with electrospray tandem mass spectrometry to analyze the acidic MOs in rat and mouse. Among the fifteen MOs identified, twelve were reported for the first time in rat and mouse together with two novel sulphated oligosaccharides. The complete list of acidic oligosaccharides present in rat and mouse milk is the baseline information of these animals and should contribute to biological/biomedical studies using rats and mice as models.

Regulation of Gut Microbiota Disrupts the Glucocorticoid Receptor Pathway and Inflammation-related Pathways in the Mouse Hippocampus.

An increasing number of studies have recently indicated the important effects of gut microbes on various functions of the central nervous system. However, the underlying mechanisms by which gut microbiota regulate brain functions and behavioral phenotypes remain largely unknown. We therefore used isobaric tags for relative and absolute quantitation (iTRAQ)-based quantitative proteomic analysis to obtain proteomic profiles of the hippocampus in germ-free (GF), colonized GF, and specific pathogen-free (SPF) mice. We then integrated the resulting proteomic data with previously reported mRNA microarray data, to further explore the effects of gut microbes on host brain functions. We identified that 61 proteins were upregulated and 242 proteins were downregulated in GF mice compared with SPF mice. Of these, 124 proteins were significantly restored following gut microbiota colonization. Bioinformatic analysis of these significant proteins indicated that the glucocorticoid receptor signaling pathway and inflammation-related pathways were the most enriched disrupted pathways. This study provides new insights into the pathological mechanisms of gut microbiota-regulated diseases.

Arecanut (Areca catechu L.) Seed Polyphenol-Ameliorated Osteoporosis by Altering Gut Microbiome via LYZ and the Immune System in Estrogen-Deficient Rats.

Polyphenol can improve osteoporosis and is closely associated with gut microbiota, while the mechanism and the relationship among polyphenol, osteoporosis, and gut microbiota colonization remain unclear. Here, an osteoporosis rat model established by ovariectomy was employed to investigate the improving mechanism of arecanut (Areca catechu L.) seed polyphenol (ACP) on osteoporosis by regulating gut microbiota. We analyzed the bone microstructure, Paneth cells, regulating microbial protein (lysozyme (LYZ)), proinflammatory cytokines, macrophage infiltration levels, and gut microbial communities in a rat. ACP improved the trabecular microstructure compared to OVX, including the increased trabecular number (Tb.N) (P < 0.01) and trabecular thickness (Tb.Th) (P < 0.001) and decreased trabecular separation (Tb.Sp) (P < 0.01). At the phylum level, Bacteroidetes was increased after ovariectomy (P < 0.001) and Firmicutes and Proteobacteria were increased in ACP (P < 0.001). Antiosteoporosis groups with lower LYZ and Paneth cells (P < 0.001) showed that the microbiota Alistipes, which have a negative effect on bone metabolism were decreased in ACP (P < 0.001). Altogether, these studies showed that the estrogen deficiency could induce the shedding of Paneth cells, which leads to the decrease of LYZ, while ACP could increase the LYZ expression by maintaining the population of Paneth cells in an estrogen-deficient host, which were implicated in gut microbiota regulation and improved osteoporosis by controlling the inflammatory reaction.

Perturbations of gut microbiota in gestational diabetes mellitus patients induce hyperglycemia in germ-free mice.

Shifts in the maternal gut microbiota have been implicated in the development of gestational diabetes mellitus (GDM). Understanding the interaction between gut microbiota and host glucose metabolism will provide a new target of prediction and treatment. In this nested case-control study, we aimed to investigate the causal effects of gut microbiota from GDM patients on the glucose metabolism of germ-free (GF) mice. Stool and peripheral blood samples, as well as clinical information, were collected from 45 GDM patients and 45 healthy controls (matched by age and prepregnancy body mass index (BMI)) in the first and second trimester. Gut microbiota profiles were explored by next-generation sequencing of the 16S rRNA gene, and inflammatory factors in peripheral blood were analyzed by enzyme-linked immunosorbent assay. Fecal samples from GDM and non-GDM donors were transferred to GF mice. The gut microbiota of women with GDM showed reduced richness, specifically decreased Bacteroides and Akkermansia, as well as increased Faecalibacterium. The relative abundance of Akkermansia was negatively associated with blood glucose levels, and the relative abundance of Faecalibacterium was positively related to inflammatory factor concentrations. The transfer of fecal microbiota from GDM and non-GDM donors to GF mice resulted in different gut microbiota colonization patterns, and hyperglycemia was induced in mice that received GDM donor microbiota. These results suggested that the shifting pattern of gut microbiota in GDM patients contributed to disease pathogenesis.

Abstract P112: Elevated Blood Pressure In Conventionalized Germ-free Rats Is Coupled With Upregulation Of Kynurenic Pathway Metabolites And Central Immune Responses

Background: Recent evidence supports that metabolic dysfunction underlies hypertension. Injection of kynurenate, a metabolite of tryptophan pathway, into the paraventricular nucleus of the hypothalamus (PVN) lowers blood pressure (BP). Intestinal absorption and metabolism of tryptophan are impacted by gut microbiota. Since gut-brain axis contributes to gut dysbiosis-inducd hypertension, we hypothesized that gut microbiota modulates the levels of kynurenic pathway metabolites that have central impact on BP regulation. Methods: We, for the first time, used 7 weeks old male Germ-free (GF) Spague Dawley (SD) rats (n=5) and GF rats co-housed with conventional SD rats for 10 days (GFC) (n=6). BP was measured by tail-cuff. Serum metabolites were quantified by 6495 triple quandrople mass spectrometryand data was normalized using isotoplic labelled compounds. The nucleus of the solitary tract (NTS), the principal sensory nucleus for peripheral changes, and the PVN, a relay center projecting sympathetic output based on the integrated afferent inputs from brain regions including NTS, were analyzed by microarray hybridization for mRNA expression. Results: Compared to the GF rats, GFC rats had significantly higher systolic (139 mmHg vs 115 mmHg, p &lt;0.05), diastolic BP (96 mmHg vs 79 mmHg, p &lt;0.05), and serum levels of kynurenic acid (-9.76 vs -10.21, p &lt;0.05) and 3-hydroxy kynurenine (-6.49 vs -7.34, p &lt;0.01). Coupled with these increases in kynurenic pathway metabolites, microarray analyses demonstrated increased immune responses (e.g. Cd74, Il1b, Cxcl1, Mmp14 ) in the PVN (gene ontology analysis, p &lt;0.001) and increased cell differentiation and synaptic plasticity (e.g. Sox11, Tp53, Cdk6, Hoxb4, Foxo4, Cyr61 ) in the NTS (gene ontology analysis, p &lt;0.01). Conclusion: Colonization of gut microbiota in GF rats induced increased cell differentiation and synaptic plasticity in the NTS and immune responses in the PVN, indicating the restructured sensory neurons of the NTS and enhanced sympathetic output from the PVN. These are in line with increased levels of kynurenic acid and 3-hydroxy kynurenine, and BP, respectively, suggesting that BP regulation by the gut-brain axis may be mediated by kynurenic pathway.

Enduring Behavioral Effects Induced by Birth by Caesarean Section in the Mouse

Birth by Caesarean (C)-section impacts early gut microbiota colonization and is associated with an increased risk of developing immune and metabolic disorders. Moreover, alterations of the microbiome have been shown to affect neurodevelopmental trajectories. However, the long-term effects of C-section on neurobehavioral processes remain unknown. Here, we demonstrated that birth by C-section results in marked but transient changes in microbiome composition in the mouse, in particular, the abundance of Bifidobacterium spp. was depleted in early life. Mice born by C-section had enduring social, cognitive, and anxiety deficits in early life and adulthood. Interestingly, we found that these specific behavioral alterations induced by the mode of birth were also partially corrected by co-housing with vaginally born mice. Finally, we showed that supplementation from birth with a Bifidobacterium breve strain, or with a dietary prebiotic mixture that stimulates the growth of bifidobacteria, reverses selective behavioral alterations in C-section mice. Taken together, our data link the gut microbiota to behavioral alterations in C-section-born mice and suggest the possibility of developing adjunctive microbiota-targeted therapies that may help to avert long-term negative consequences on behavior associated with C-section birth mode.

The crucial role of early-life gut microbiota in the development of type 1 diabetes.

Early-life healthy gut microbiota has a profound implication on shaping the mucosal immune system as well as maintaining healthy status later in life, especially at the prenatal or neonatal stages, while intestinal dysbiosis in early life is associated with several autoimmune diseases, including type 1 diabetes (T1D). Since the gut microbiome is potentially modifiable, optimizing the intestinal bacterial composition in early life may be a novel option for T1D prevention. In this review, we will review current data depicting the crucial role of early-life intestinal microbiome in the development of T1D and discuss the possible mechanisms whereby early-life intestinal microbiome influences the T1D progression. We also summarize recent findings on environmental factors affecting gut microbiota colonization and interventions that may successfully alter microbial composition to discuss potential means of preventing T1D progression in at-risk children.

1．肥満・糖尿病の病態と腸内細菌叢 1）新生児・乳幼児期の腸内細菌叢の構築―出生早期の腸内細菌叢構築とその後の非感染性疾患リスクとの関連―

1．肥満・糖尿病の病態と腸内細菌叢 1）新生児・乳幼児期の腸内細菌叢の構築―出生早期の腸内細菌叢構築とその後の非感染性疾患リスクとの関連―

Integrative Review of Gut Microbiota and Expression of Symptoms Associated With Neonatal Abstinence Syndrome.

Neonatal exposure and subsequent withdrawal from maternal substance use disorder are a growing problem and consequence of the current opioid epidemic. Neonatal abstinence syndrome (NAS) is defined by a specified cluster of symptoms with treatment guided by the expression and severity of these symptoms. The mechanisms or pathophysiology contributing to the development of NAS symptoms are not well known, but one factor that may influence NAS symptoms is the gut microbiota. The purpose of this integrative review was to examine evidence that might show if and how the gut microbiota influence expression and severity of symptoms similar to those seen in NAS. Using published guidelines, a review of research studies that focused on the gut microbiome and symptoms similar to those seen in NAS was conducted, using the Cochrane, EMBASE, and Scopus databases, from 2009 through 2019. The review results included findings of aberrant microbial diversity, differences in microbial communities between study groups, and associations between specific taxa and symptoms. In studies involving interventions, there were reports of improved microbial diversity, community structure, and symptoms. The review findings provide evidence that the gut microbiota may play a role in modifying variability in the expression and severity of symptoms associated with NAS. Future research should focus on examining the gut microbiota in infants with and without the syndrome as well as exploring the relationship between symptom expression and aberrant gut microbiota colonization in infants with NAS.

Postnatal Gut Immunity and Microbiota Development Is Minimally Affected by Prenatal Inflammation in Preterm Pigs.

Chorioamnionitis (CA), resulting from intra-amniotic inflammation, is a frequent cause of preterm birth and exposes the immature intestine to bacterial toxins and/or inflammatory mediators before birth via fetal swallowing. This may affect intestinal immune development, interacting with the effects of enteral feeding and gut microbiota colonization just after birth. Using preterm pigs as model for preterm infants, we hypothesized that prenatal exposure to gram-negative endotoxin influences postnatal bacterial colonization and gut immune development. Pig fetuses were given intra-amniotic lipopolysaccharide (LPS) 3 days before preterm delivery by cesarean section and were compared with littermate controls (CON) at birth and after 5 days of formula feeding and spontaneous bacterial colonization. Amniotic fluid was collected for analysis of leukocyte counts and cytokines, and the distal small intestine was analyzed for endotoxin level, morphology, and immune cell counts. Intestinal gene expression and microbiota were analyzed by transcriptomics and metagenomics, respectively. At birth, LPS-exposed pigs showed higher intestinal endotoxin, neutrophil/macrophage density, and shorter villi. About 1.0% of intestinal genes were affected at birth, and DMBT1, a regulator of mucosal immune defense, was identified as the hub gene in the co-expression network. Genes related to innate immune response (TLR2, LBP, CD14, C3, SFTPD), neutrophil chemotaxis (C5AR1, CSF3R, CCL5), and antigen processing (MHC II genes and CD4) were also affected, and expression levels correlated with intestinal neutrophil/macrophage density and amniotic fluid cytokine levels. On day 5, LPS and CON pigs showed similar sensitivity to necrotizing enterocolitis, endotoxin levels, morphology, immune cell counts, gene expressions, and microbiota composition (except for difference in some low-abundant species). Our results show that CA markedly affects intestinal genes at preterm birth, including genes related to immune cell infiltration. However, a few days later, following the physiological adaptations to preterm birth, CA had limited effects on intestinal structure, function, gene expression, bacterial colonization, and necrotizing enterocolitis sensitivity. We conclude that short-term, prenatal intra-amniotic inflammation is unlikely to exert marked effects on intestinal immune development in preterm neonates beyond the immediate neonatal period.

Perinatal Antibiotic Exposure Affects the Transmission between Maternal and Neonatal Microbiota and Is Associated with Early-Onset Sepsis

Intrapartum antibiotic prophylaxis reduces the risk of infection to a mother and neonate, but antibiotic-mediated maternal and neonatal microbiota dysbiosis increases other health risks to newborn infants. We studied the impact of perinatal antibiotic prophylaxis on the microbiota in mothers and newborns with full-term or preterm delivery. Ninety-eight pregnant women and their neonates were divided into the following four groups: full term without antibiotic exposure (FT), full term with antibiotic exposure (FTA), preterm without antibiotic exposure (PT), and preterm with antibiotic exposure (PTA). Bacterial composition was analyzed by sequencing the 16S rRNA gene from maternal vaginal swabs (V) and neonatal meconium (F). The results showed that in maternal vaginal and neonatal meconium microbiota, FT and PT groups had a higher load of Lactobacillus spp. than did the FTA and PTA groups. In addition, whether in the mother or newborn, the dissimilarity in microbiota between FT and PT was the lowest compared to that between other groups. Compared to the FT and PT groups, the dissimilarity in microbial structures between the vagina and meconium decreased in the FTA and PTA groups. The health outcome of infants reveals an association between early-onset sepsis and antibiotic-mediated microbiota dysbiosis. In conclusion, perinatal antibiotic exposure is related to the establishment of gut microbiota and health risks in newborns. Promoting the rational usage of antibiotics with pregnant women will improve neonatal health.IMPORTANCE Perinatal antibiotic prophylaxis is an effective method for preventing group B Streptococcus (GBS) infection in newborns. Antibiotic exposure unbalances women's vaginal microbiota, which is associated with the establishment of the newborn gut microbiota. However, the influence of perinatal antibiotic exposure on neonatal gut microbiota colonization and health outcomes remains unclear. In this study, we found that perinatal antibiotic exposure induced microbiota dysbiosis in a woman's vagina and the neonatal gut, and we highlight a significant decrease in the abundance of Lactobacillus spp. The influence of antibiotic use on the microbiota was greater than that from gestational age. Additionally, full-term newborns without antibiotic exposure had no evidence of early-onset sepsis, whereas in full-term or preterm newborns with antibiotic exposure before birth, at least one infant was diagnosed with early-onset sepsis. These results suggest an association between perinatal antibiotic exposure and microbial dysbiosis in maternal vaginal and neonatal gut environments, which may be related to the occurrence of early-onset sepsis.

Goat Milk Consumption Enhances Innate and Adaptive Immunities and Alleviates Allergen-Induced Airway Inflammation in Offspring Mice.

Goat milk (GM), as compared to cow milk (CM), is easier for humans to digest. It also has antioxidant and anti-inflammatory effects and can improve minor digestive disorders and prevent allergic diseases in infants. It is unclear whether GM consumed in pregnant mothers has any protective effects on allergic diseases in infants. In this experimental study with mice, we found GM feeding enhanced immunoglobulin production, antigen-specific (ovalbumin, OVA) immune responses, and phagocytosis activity. The GM-fed mice had an increasing proportion of CD3+ T lymphocytes in the spleen. Splenocytes isolated from these animals also showed significantly increased production of cytokines IFN-γ and IL-10. More importantly, GM feeding during pregnancy and lactation periods can confer protective activity onto offspring by alleviating the airway inflammation of allergic asthma induced by mite allergens. There was a remarkably different composition of gut microbiota between offspring of pregnant mice fed with water or with milk (GM or CM). There was a greater proportion of beneficial bacterial species, such as Akkermansia muciniphila, Bacteroides eggerthii, and Parabacteroides goldsteinii in the gut microbiota of offspring from GM- or CM-fed pregnant mice compared to the offspring of water-fed pregnant mice. These results suggested that improving the nutrition of pregnant mice can promote immunological maturation and colonization of gut microbiota in offspring. This mother-to-child biological action may provide a protective effect on atopy development and alleviate allergen-induced airway inflammation in offspring.

Absence of gut microbiota affects lipid metabolism in the prefrontal cortex of mice

ABSTRACTObjectives: Lipid metabolism is closely associated with many important biological functions. Here, we conducted this study to explore the effects of gut microbiota on the lipid metabolism in the prefrontal cortex of mice.Methods: Germ-free (GF) mice, specific pathogen-free (SPF) and colonized GF (CGF) mice were used in this study. The open field test (OFT), forced swimming test (FST) and novelty suppressed feeding test (NSFT) were conducted to assess the changes in general behavioral activity. The liquid Chromatography-Tandem Mass Spectrometry (LC-MS/MS) was used to obtain the lipid metabolites. Both one-way analysis of variance (one-way ANOVA) and orthogonal partial least-squares discriminant analysis (OPLS-DA) were used to obtain the key differential lipid metabolites.Results: The behavioral tests showed that compared to SPF mice, GF mice had more center distance, more center time, less immobility time and less latency to familiar food. Meanwhile, 142 key differential lipid metabolites between SPF mice and GF mice were identified. These lipid metabolites mainly belonged to glycerophospholipids, glycerolipids, sphingolipids, and saccharolipids. The gut microbiota colonization did not reverse these changed behavioral phenotypes, but could restore 25 key differential lipid metabolites.Discussion: These results showed that the absence of gut microbiota could influence host behaviors and lipid metabolism. Our findings could provide original and valuable data for future studies to further investigate the microbiota-gut-brain axis.

Short communication: Gut microbial colonization of the mouse colon using faecal transfer was equally effective when comparing rectal inoculation and oral inoculation based on 16S rRNA sequencing

In the present study we hypothesized that a higher degree of gut microbiota (GM) transfer and colonization could be reached by rectal inoculation compared to oral inoculation, which is commonly used in mouse studies for GM transfer. We treated C57BL/6NTac Specific Pathogen Free (SPF) mice with antibiotics and subsequently we inoculated these with GM from donor mice of the same strain by either the oral or the rectal inoculation method. 16S rRNA gene sequencing of the colon microbiota showed no difference in microbial community on account of inoculation method as determined by unweighted UniFrac distance metrics in C57BL/6NTac SPF mice. In addition, qPCR analysis on colon tissue revealed no difference in mRNA expression between the inoculation methods. Next, the SPF mice were compared to germ-free (GF)-mice to identify differences in inoculation efficacy. Whether the mice were antibiotic treated SPF or GF clearly influenced GM determined by 16S rRNA gene sequencing where the SPF mice experienced up-regulation of S24–7 (p = .0001) and a decrease in Rikenellaceae (p = .016) compared to GF mice. qPCR analysis on colon tissue revealed up-regulation in mRNA gene expression of Il6, Il10, Reg3g and transcription factor RORγt (Rorc) in GF mice compared to SPF mice on a significant level (p < .05). This gene expression profile is consistent with post colonization development of the intestinal barrier in GF mice.