Background:The gut microbiota is a significant reservoir of antimicrobial resistance genes (ARGs). The use and misuse of antimicrobials can select multi-resistant bacteria and modify the repertoire of ARGs in the gut. Developing effective interventions to manipulate the intestinal resistome would allow us to modify the antimicrobial resistance risk. Materials and Methods:Applying shotgun metagenomics, we compared the composition of fecal resistome from individuals treated with triple therapy for Helicobacter pylori plus Saccharomyces boulardii CNCM-I 745 (Sb) versus triple antibiotherapy without S. boulardii (control) before, after, and one month after treatments. DNA samples were sequenced on an Illumina NovaSeq 6000 platform. Reads were trimmed and filtered for quality, and the reads classified as host genome were removed from further analysis. We used the ResFinder database for resistome analysis and the web-based tool ResistoXplorer and RStudio for graphical representation and statistical analysis. Results:We identified 641 unique ARGs in all fecal samples, conferring resistance to 18 classes of antibiotics. The most prevalent ARGs found in at least 90% of the samples before the treatments were against tetracyclines, MLS-B (macrolide, lincosamide, and streptogramin B), beta-lactams, and aminoglycosides. Differential abundance analysis allowed the identification of ARGs significantly different between treatment groups. Thus, immediately after the treatments, the abundance of ARGs that confer resistance to lincosamides, tetracyclines, MLS-B, and two genes in the beta-lactam class (cfxA2 and cfxA3) was significantly lower in the group that received Sb than in the control group (edgeR, FDR <0.05). Conclusion:Our study demonstrated that the addition of S. boulardii CNCM-I 745 to the conventional antibiotic eradication therapy for H. pylori reduced the abundance of ARGs, particularly those genes that confer resistance to lincosamides, tetracyclines, MLS-B, and a few genes in the beta-lactams class.

Probiotic bacteria are frequently used to treat intestinal diseases or to improve health; however, little is known about the evolutionary changes of these bacteria during probiotic manufacture and the bacterial ability to colonize the intestine. It has been observed that when bacteria adapt to a new environment, they lose some traits required to thrive in the original niche. In this study, a strain of Lactobacillus reuteri was isolated from mouse duodenum and subjected to 150 serial passes in milk to simulate the industrial propagation of probiotic bacteria. The strains adapted to milk outperformed their ancestor when grown in milk; we also showed evidence of reduced intestinal colonization of milk‐adapted strains. Whole‐genome sequencing showed that bacterial adaptation to milk selects mutants with altered metabolic functions.

Probiotic bacteria are frequently used to treat intestinal diseases or to improve health; however, little is known about the evolutionary changes of these bacteria during probiotic manufacture and the bacterial ability to colonize the intestine. It has been observed that when bacteria adapt to a new environment, they lose some traits required to thrive in the original niche. In this study, a strain of Lactobacillus reuteri was isolated from mouse duodenum and subjected to 150 serial passes in milk to simulate the industrial propagation of probiotic bacteria. The strains adapted to milk outperformed their ancestor when grown in milk; we also showed evidence of reduced intestinal colonization of milk‐adapted strains. Whole‐genome sequencing showed that bacterial adaptation to milk selects mutants with altered metabolic functions.

The gastrointestinal tract constitutes a complex and diverse ecosystem. Escherichia coli is one of the most frequently studied and characterized species in the gut ecosystem, nevertheless, there has been little research to determine their diversity and population dynamics in the intestines of children over time. In this prospective study, a fresh fecal sample was obtained from children longitudinally over one year (30 fecal samples at sampling period 1 and 22 fecal samples at sampling periods 2 and 3). From each stool sample, five E. coli colonies were randomly selected (n = 405 E. coli isolates total) in order to characterize the genotype and phenotypic antimicrobial resistance patterns. We found that all numerically dominant E. coli lineages in children's intestines were transient colonizers, and antimicrobial resistance phenotypes of these strains varied significantly over time without any apparent selective force. Whole-genome sequencing of 3 isolates belonging to ST131 found in one child during the sampling period I and II indicated that isolates were three different ST 131 clones that carried extended-spectrum β-lactamase (ESBL) genes.