BackgroundAntibiotics, as the most commonly prescribed class of drugs in neonatal intensive care units, have an important impact on the developing neonatal gut microbiota. Therefore, comprehending the effects of commonly used antibiotic therapy on the gut microbiota and butyrate-producers in early infants could provide information for therapeutic decision-making in the NICU.ObjectivesTo explore the effects of antibiotic therapy on the early development of gut microbiota and butyrate-producers in early infants.MethodsA total of 72 infants were included in the study. We performed 16S rRNA sequencing on stool swab samples collected from neonatal intensive care unit patients who received amoxicillin-clavulanic acid (AC, n = 10), moxalactam (ML, n = 28) and non-antibiotics (NA, n = 34). We then compared the taxonomic composition between treatment regimens, focusing on differences in butyrate-producers.ResultsOur study showed that there were significant differences in Shannon index (p = 0.033) and Beta diversity (p = 0.014) among the three groups. At the family level, compared with the other two groups, the relative abundance of Clostridiaceae (p < 0.001) and Veillonellaceae (p = 0.004) were significantly higher, while the relative abundance of Enterococcidae (p < 0.001) was significantly lower in the NA group. The relative abundance of Enterobacteriaceae (p = 0.022) in the AC group was greater than that in the other two groups. Additionally, butyrate-producers (p < 0.001), especially Clostridiaceae (p < 0.001), were noticeably more abundant in the NA group. The relative abundance of Clostridiaceae and butyrate-producers were the lowest in the ML group (p < 0.001).ConclusionWe found that antibiotic therapy had an adverse impact on the initial development of gut microbiota and leaded to a reduction in the abundance of butyrate-producers, particularly Clostridiaceae. Furthermore, moxalactam had a more pronounced effect on the gut microbiota compared to amoxicillin-clavulanic acid.

Exposure to chemical pollutants and their effects on the gut microbiome during early life are scarce, especially the effects of mixed exposures. Plasma pollutants levels were measured using gas chromatography -triple quadrupole mass spectrometer (GC-MS/MS) among 304 infants in the neonatal ward at Hunan Children's hospital, China, and gut microbiota was derived from 16S rRNA sequencing. We assessed exposure and alpha diversity using generalized linear models, and variation in beta diversity (Bray-Curtis), taxa abundance (MaAsLin2), and employed Bayesian kernel machine regression (BKMR) to investigate the association of pollutants mixture with alpha diversity and taxa. PBDE-99 was positively associated with the Chao1 index (beta = 4.29, 95%CI:1.54,7.03). Exposure to the pesticides trifluralin, gamma-BHC, and methidathion significantly affected beta diversity (all P-FDR < 0.05). PBDE-100, beta-BHC, phosalone, methiamitron, fenpropathrin, delta-BHC, and o,p'-DDT were associated with changes in taxa abundance, including negative associations [e.g., Staphylococcus, Bacteroides, Bifidobacterium, and Corynebacterium] and positive associations [e.g., Acinetobacter and Pseudomonas]. An interaction between o,p'-DDT and delta-BHC on Pseudomonas was also found in BKMR models. Our findings suggest that chemical pollutants are associated with gut microbiome changes in hospitalized infants, providing new insights into the mechanisms of chemical pollutants toxicity. Further validation is necessary to confirm these associations and explore their long-term health effects.

Previous research has found a correlation between heavy metals and gut microbiota in humans. However, there are few population-based studies examining the impact of early life thallium (Tl) exposure on neonatal microbiome. 342 newborns were recruited from Hunan Children's Hospital and subsequently divided into three groups (low, medium, and high) based on the 25th and 75th percentiles of serum Tl concentration. Additionally, the relationship between Tl and gut microbiota was analyzed in subgroups (preterm or full-term neonates). The association between Tl and gut microbiota in neonates was analyzed by Redundancy analysis, Spearman correlation analysis and MaAsLin2. The detection rate of Tl in neonates was 100%, with the median concentration of 0.021 mu g/L. In all neonates, we found significant differences in the Chao1 and ACE indices of alpha-diversity in gut microbiota, and the relative abundances of Bacteroidota and Bacteroidetes were significantly different among groups (p < 0.05). Following the covariate adjustment, Tl was negatively correlated with Gemmatimonadota (Coef = 0.265, p < 0.05) in preterm neonates. In full-term neonates, Tl exhibited a positive correlation with the relative abundance of Robinsoniella (Coef = 0.563, p = 0.009) and a negative correlation with that of Pseudomonas (Coef = - 0.592, p = 0.012). Tryptophan and renin-angiotensin system pathways might exert important roles in Tl exposure. This study indicated that Tl exposure was associated with changes in alpha-diversity and the composition of gut microbiota in neonates, with Gemmatimonadota being predominantly affected in preterm neonates and Robinsoniella and Pseudomonas in full-term neonates.

To better understand the variations in gut microbiota in children with different types of epilepsy. Thirty-seven children with epilepsy were included in the case group, which was further divided into focal (group A, n = 28) and generalized epilepsy groups (group B, n = 9) based on the origin and extent of the seizures. The focal epilepsy group was subdivided into the benign childhood epilepsy with centrotemporal spikes (BECT) (group C, n = 9) and non-BECT groups (group D, n = 19) based on the appearance of typical centrotemporal spikes or spike-wave complexes on the electroencephalogram (EEG). Additionally, 14 healthy children were selected as the control group (group E, n = 14). Significant differences were observed in the diversity and composition of gut microbiota between the case and control groups. At the genus level, the abundance of Megamonas (P = 0.001), Streptococcus (P<0.001), Romboutsia (P = 0.001), Bacteroides (P<0.05), and Escherichia/Shigella (P<0.05) was significantly higher in the focal epilepsy group than in the control group (0.027 vs. 0.00009, P = 0.001; 0.016 vs. 0.002, P<0.001; 0.013 vs. 0.002, P = 0.001; 0.030 vs. 0.002, P<0.05, respectively). Additionally, Escherichia/Shigella (P<0.05) was more abundant in the case group compared to the control group (0.033 vs. 0.002, P<0.05). Bacteroides (P<0.05) was more abundant in the control group than in the case group. Megamonas (P<0.001) and Collinsella (P<0.05) were significantly more prevalent in the BECT group than in the control group (0.034 vs. 0.00009, P<0.001; 0.014 vs. 0.001, P<0.05, respectively). In the non-BECT group, compared to the control group, Megamonas (P = 0.013), Streptococcus (P<0.001), Romboutsia (P = 0.001), and Escherichia/Shigella (P<0.05) were found in greater abundance (0.023 vs. 0.00009, P = 0.013; 0.018 vs. 0.002, P<0.001; 0.014 vs. 0.002, P = 0.001; 0.037 vs. 0.002, P<0.05, respectively). Though, there were no statistically significant differences in gut microbiota between the different types of epilepsy, the gut microbiota of children with epilepsy significantly differed from that of healthy controls. The increased abundance of Escherichia/Shigella may lead to the worsening of clinical phenotypes and poor prognosis, and it could be a candidate biomarker to identify the focal epilepsy or even non-benign childhood epilepsy with centrotemporal spikes, potentially providing new therapeutic targets for the future.