A global rise in antimicrobial resistance among pathogenic bacteria has proved to be a major public health threat, with the rate of multidrug-resistant bacterial infections increasing over time. The gut microbiome has been studied as a reservoir of antibiotic resistance genes (ARGs) that can be transferred to bacterial pathogens via horizontal gene transfer (HGT) of conjugative plasmids and mobile genetic elements (the gut resistome). Advances in metagenomic sequencing have facilitated the identification of resistome modulators, including live microbial therapeutics such as probiotics and fecal microbiome transplantation that can either expand or reduce the abundances of ARG-carrying bacteria in the gut. While many different gut microbes encode for ARGs, they are not uniformly distributed across, or transmitted by, various members of the microbiome, and not all are of equal clinical relevance. Both experimental and theoretical approaches in microbial ecology have been applied to understand differing frequencies of ARG horizontal transfer between commensal microbes as well as between commensals and pathogens. In this commentary, we assess the evidence for the role of commensal gut microbes in encoding antimicrobial resistance genes, the degree to which they are shared both with other commensals and with pathogens, and the host and environmental factors that can impact resistome dynamics. We further discuss novel sequencing-based approaches for identifying ARGs and predicting future transfer events of clinically relevant ARGs from commensals to pathogens.
The multicellular haploid generation of plants (gametophyte) is responsible for sperm and egg production. In the fern Ceratopteris richardii , gametophytes are free-living and may develop into either males or hermaphrodites. This developmental decision is not genetically programmed, but instead is environmentally determined. A pheromone released by hermaphrodites called antheridiogen induces individuals to develop as males. The presence of the bacterium Pseudomonas nitroreducens blocks male induction and results in more individuals developing as hermaphrodites. The bacterium also induces longer but fewer rhizoids to develop in both males and hermaphrodites.
Historically, investigators have assumed microorganisms identified in mother’s milk to be contaminants, but recent data suggest that milk microbiota may contribute to beneficial maternal effects. Microorganisms that colonize the gastrointestinal tracts of newborn mammals are derived, at least in part, from the maternal microbial population. Milk-derived microbiota is an important source of this microbial inocula and we hypothesized that the maternal diet contributes to variation in this microbial community. To evaluate the relationship between a mother’s diet and milk microbiome, we fed female rats a low- or high-protein diet and mated all individuals. Milk and cecal contents were collected from dams at peak lactation (14-day post-partum), and the bacterial composition of each community was assessed by 16S rRNA gene amplicon sequencing. Our findings revealed higher dietary protein intake decreased fecal microbial diversity but increased milk microbial and pup cecum diversity. Further, the higher dietary protein intake resulted in a greater abundance of potentially health-promoting bacteria, such as Lactobacillus spp. These data suggest that dietary protein levels contribute to significant shifts in the composition of maternal milk microbiota and that the functional consequences of these changes in microbial inocula might be biologically important and should be further explored.
Due to its immunomodulatory potential, the intestinal microbiota has been implicated as a contributing factor in the development of the meta-inflammatory state that drives obesity-associated insulin resistance and type 2 diabetes. A better understanding of this link would facilitate the development of targeted treatments and therapies to treat the metabolic complications of obesity. To this end, we validated and utilized a novel swine model of obesity, the Mangalica pig, to characterize changes in the gut microbiota during the development of an obese phenotype, and in response to dietary differences. In the first study, we characterized the metabolic phenotype and gut microbiota in lean and obese adult Mangalica pigs. Obese or lean groups were created by allowing either ad libitum (obese) or restricted (lean) access to a standard diet for 54 weeks. Mature obese pigs were significantly heavier and exhibited 170% greater subcutaneous adipose tissue mass, with no differences in muscle mass compared to their lean counterparts. Obese pigs displayed impaired glucose tolerance and hyperinsulinemia following oral glucose challenge, indicating that a metabolic phenotype also manifested with changes in body composition. Consistent with observations in human obesity, the gut microbiota of obese pigs displayed altered bacterial composition. In the second study, we characterized the longitudinal changes in the gut microbiota in response to diet and aging in growing Mangalica pigs that were either limit fed a standard diet, allowed ad libitum access to a standard diet, or allowed ad libitum access to a high fat-supplemented diet over an 18-week period. As expected, weight gain was highest in pigs fed the high fat diet compared to ad libitum and limit fed groups. Furthermore, the ad libitum and high fat groups displayed significantly greater adiposity consistent with the development of obesity relative to the limit fed pigs. The intestinal microbiota was generally resilient to differences in dietary intake (limit fed vs ad libitum), though changes in the microbiota of pigs fed the high fat diet mirrored changes observed in mature obese pigs during the first study. This is consistent with the link observed between the microbiota and adiposity. In contrast to intestinal bacterial populations, bacteriophage populations within the gut microbiota responded rapidly to differences in diet, with significant compositional changes in bacteriophage genera observed between the dietary treatment groups as pigs aged. These studies are the first to describe the development of the intestinal microbiota in the Mangalica pig, and are the first to provide evidence that changes in body composition and dietary conditions are associated with changes in the microbiome of this novel porcine model of obesity.
Bacterial dysbiosis as a result of nutritional, bacterial, viral, and parasitic gastrointestinal infections can adversely affect the metabolism, productivity, and overall health of cattle. The purpose of this project was to characterize the commensal microbiota present in two locations of the rumen concomitantly in vivo with the animals undergoing habitual husbandry, as it was hypothesized that there are major differences in the commensal microbiota present in the two locations of the adult bovine major forestomach. A surgically fitted rumen cannula was used to allow ruminal lumen contents and mucosal biopsies to be collected from six crossbred yearling steers. In order to assess as much environmental and individual steer microbiota variation as possible, each animal was randomly sampled three times over a 3 week period. 16S rRNA sequencing was performed to provide a detailed descriptive analysis from phylum to genus taxonomic level. Significant differences were observed between luminal and epimural bacterial populations in the bovine rumen. As expected, a core microbiome composed by Firmicutes and Bacteroidetes represented over 90% of the microbiome, however, further analysis showed distinct diversity and distribution of the microbiome between the two locations. Characterizing the gastrointestinal microbiome in vivo is imperative. The novelty and the contribution of this study to the literature is the use of live cattle which allowed real-time sample collections and analysis of the rumen microbiome providing an understanding of what is normal in the live animal.
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