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New Strategies to Discover Non-Ribosomal Peptides as a Source of Antibiotics Molecules
Published in Peter Grunwald, Pharmaceutical Biocatalysis, 2019
Mario Alberto Martínez-Núñez, Zuemy Rodríguez-Escamilla, Víctor López y López
Through molecular elements such as enzymes or efflux pumps, bacteria have been able to contend against the antibiotics of other bacteria, which allows them to increase their population in the different environments they inhabit, i.e., land, water, or be associated to other organisms. Being able to compete for the colonization of the same or different ecological niches as an adaptive strategy, antibiotic resistance is an ancient, diverse, and widely distributed mechanism (Pawlowski et al., 2016). This group of molecular elements that allow bacteria to resist antibiotics is now known as the resistome, and its presence in ancient natural environments has been proven, for example, in frozen sediments of 30,000 years old, predating the modern use of antibiotics as drugs (D’Costa et al., 2011). The resistome comprises all genes present in a bacterial genome or in a group of bacterial genomes (pan-genome) that live in a given environment and confer antibiotic resistance to the bacterial population not only to clinical pathogenic bacteria, but also to the non-pathogenic species (Wright, 2007; Perry et al., 2014). This collection of resistance genes encompasses both intrinsic and acquired resistance genes, as well as proto-resistance genes and silent or cryptic resistance genes that have moved across environment and bacterial species through mobile elements such as plasmids or transposons that facilitate the horizontal gene transfer of the resistome (Perry et al., 2014; Hu et al., 2016). The resistome profile can vary between different environments, for example, in water environments, including sewage, hospital and animal production wastewaters, ground water, surface water, drinking water, and so on. The most frequently genes are tet genes encoding resistance to tetracyclines, aac, aph, and ant genes to aminoglycosides, and a variety of bla genes to β-lactams. In marine environments, resistome profile changes, with an abundance of genes that confer resistance to ampicillin, tetracycline, nitrofurantoin, and sulfadimethoxine (Hu et al., 2017). The host- associated environments such as gut microbiota in humans and farm animals, have a more complex resistome profile because to the more frequent exposure to antibiotics. In farm pigs from different countries the genes coding for resistance to bacitracin, cephalosporin, macrolide, streptogramin B and tetracycline are prevalent (Xiao et al., 2016), while in the human gut microbiota of Chinese individuals, the tetracycline resistance gene tet showed the highest abundance (Hu et al., 2014). An analysis of resistome present in more than 600 bacterial genomes found that the environmental and human-associated microbial communities harbor distinct antibiotic-resistant genes; therefore resistome profile may be clustered by ecology (Gibson et al., 2015), while transfer of mobile resistome in bacteria is mainly controlled by phylogeny (Hu et al., 2016).
The double-edged sword of probiotic supplementation on gut microbiota structure in Helicobacter pylori management
Published in Gut Microbes, 2022
Ali Nabavi-Rad, Amir Sadeghi, Hamid Asadzadeh Aghdaei, Abbas Yadegar, Sinéad Marian Smith, Mohammad Reza Zali
Antibiotic treatment as a major disrupter of the gastrointestinal microbial community may lead to alpha diversity reduction, metabolome alteration, and antibiotic resistance.122 Antibiotic administration not only influences the resistome of the subject to whom it is given, but also the whole population owing to selection for resistance to its function.123 The propagation and spread of antibiotic resistance genes in the mucus layer is a defensive function for gut microbiota to minimize the effect of antibiotics, yet short-term antibiotic therapy can cause a long-term reduction in certain commensal bacteria.124 In addition to the antibiotic-directed modification of the gut microbiota, researchers have reported that intervention therapies can remodel the gene expression and overall metabolic activity of the gastrointestinal microbiota.125 Moreover, PPIs as essential drugs in H. pylori eradication can directly disrupt microbial composition, in addition to increasing the stomach pH and thereby influencing which bacteria reach the intestine.126 It is also suggested that the gut microbiota response to antibiotic treatment is determined by particular bacteria in the pre-treatment microbiome; thereby, targeting these bacteria may reduce the risk of dysbiosis and antibiotic-related metabolic disorders.127
Antibiotic-driven intestinal dysbiosis in pediatric short bowel syndrome is associated with persistently altered microbiome functions and gut-derived bloodstream infections
Published in Gut Microbes, 2021
Robert Thänert, Anna Thänert, Jocelyn Ou, Adam Bajinting, Carey-Ann D. Burnham, Holly J. Engelstad, Maria E. Tecos, I. Malick Ndao, Carla Hall-Moore, Colleen Rouggly-Nickless, Mike A. Carl, Deborah C. Rubin, Nicholas O. Davidson, Phillip I. Tarr, Barbara B. Warner, Gautam Dantas, Brad W. Warner
As antibiotic exposure shapes resistome enrichment and composition,16,17 we hypothesized that frequent antibiotic exposure in SBS patients would diversify and enrich the resistome. Indeed, we observed an increased abundance of ARGs and restructuring of the resistome composition in SBS patients compared to preterm and term cohorts. However, we did not find the resistome to be more diverse or enriched for a greater quantity of unique ARGs compared to the preterm and term cohorts. This indicates that an increased abundance of pathobionts, previously associated with increased ARG abundance,35 is likely the main determinant of the increased abundance of ARGs in SBS. Current enteral nutrition, associated with altered taxonomic composition of the SBS microbiota, was negatively correlated with ARG abundance, supporting the idea that taxonomy and resistome in SBS are connected in early life.
The association between early life antibiotic use and allergic disease in young children: recent insights and their implications
Published in Expert Review of Clinical Immunology, 2018
Chinwe V. Obiakor, Hein M. Tun, Sarah L. Bridgman, Marie-Claire Arrieta, Anita L. Kozyrskyj
Through meta-analytic synthesis of the literature, accumulating evidence continues to support earlier findings of association between infant antibiotic treatment, especially with multiple courses and/or broad-spectrum antibiotics, and the development of allergic disease. Many studies are able to show independence of this association from reverse causation and other early life factors. More recently published studies on large infant populations report associations with the antibiotic treatment of conditions, i.e. urinary tract infection, which do not precede allergic disease. However, reducing bias from confounding by indication for the antibiotic prescription remains a challenge even in these types of studies, with emerging evidence that susceptibility to infection is a pathway to atopy. In the meantime, increasing evidence that early changes in the gut microbiome, mycobiome, or even resistome are associated with the development of allergic disease may provide a closer link to antibiotic treatment or refute it as a cause of disease development. Greater study of the resistome will also provide further evidence on the impact of widespread use of antibiotics in infant populations on the development of antibiotic resistance. In the end, this scientific evidence will promote establishment of antibiotic stewardship programs targeted at infants and young children in hospital and community settings alike, to reduce exposure during this vulnerable time of human development [111].