mSystems最新文献

Phylogenetic marker gene sequencing is often used as a quick and cost-effective way of evaluating microbial composition within a community. While 16S rRNA gene sequencing (16S) is commonly used for bacteria and archaea, other marker genes are preferable in certain situations, such as when 16S sequences cannot distinguish between taxa within a group. Another situation is when researchers want to study cospeciation of host taxa that diverged much more recently than the slowly evolving 16S rRNA gene. For example, the bacterial gyrase subunit B (gyrB) gene has been used to investigate cospeciation between the microbiome and various hominid species. However, to date, only primers that generate short-read Illumina MiSeq-length amplicons exist to investigate gyrB of the Bacteroidaceae, Bifidobacteriaceae, and Lachnospiraceae families. Here, we update this methodology by creating gyrB primers for the Bacteroidaceae, Bifidobacteriaceae, and Lachnospiraceae families for long-read PacBio sequencing and characterize them against established short-read gyrB primer sets. We demonstrate both bioinformatically and analytically that these longer amplicons offer more sequence space for greater taxonomic resolution, lower off-target amplification rates, and lower error rates with PacBio CCS sequencing versus established short-read sequencing. The availability of these long-read gyrB primers will prove to be integral to the continued analysis of cospeciation between bacterial members of the gut microbiome and recently diverging host species.

Importance: Previous studies have shown that the marker gene gyrase subunit B (gyrB) can be used to study codiversification between the gut microbiome and hominids. However, only primers for short-read sequencing have been developed which have limited resolution for subspecies assignment. In the present study, we create new gyrB primer sets for long-read sequencing approaches and compare them to the existing short-read gyrB primers. We show that using longer reads leads to better taxonomic resolution, lower off-target amplification, and lower error rates, which are vital for accurate estimates of codiversification.

Microbial metabolism of bile acids (BAs) is crucial for maintaining homeostasis in vertebrate hosts and environments. Although certain organisms involved in bile acid metabolism have been identified, a global, comprehensive elucidation of the microbes, metabolic enzymes, and bile acid remains incomplete. To bridge this gap, we employed hidden Markov models to systematically search in a large-scale and high-quality search library comprising 28,813 RefSeq multi-kingdom microbial complete genomes, enabling us to construct a secondary bile acid production gene catalog. This catalog greatly expanded the distribution of secondary bile acid production genes across 11 phyla, encompassing bacteria, archaea, and fungi, and extended to 14 habitats spanning hosts and environmental contexts. Furthermore, we highlighted the associations between secondary bile acids (SBAs) and gastrointestinal and hepatic disorders, including inflammatory bowel disease (IBD), colorectal cancer (CRC), and nonalcoholic fatty liver disease (NAFLD), further elucidating disease-specific alterations in secondary bile acid production genes. Additionally, we proposed the pig as a particularly suitable animal model for investigating secondary bile acid production in humans, given its closely aligned secondary bile acid production gene composition. This gene catalog provides a comprehensive and reliable foundation for future studies on microbial bile acid metabolism, offering new insights into the microbial contributions to health and disease.

Importance: Bile acid metabolism is an important function in both host and environmental microorganisms. The existing functional annotations from single source pose limitations on cross-habitat analysis. Our construction of a systematic secondary bile acid production gene catalog encompassing numerous high-quality reference sequences propelled research on bile acid metabolism in the global microbiome, holding significance for the concept of One Health. We further highlighted the potential of the microbiota-secondary bile acid axis as a target for the treatment of hepatic and intestinal diseases, as well as the varying feasibility of using animal models for studying human bile acid metabolism. This gene catalog offers a solid groundwork for investigating microbial bile acid metabolism across different compartments, including humans, animals, plants, and environments, shedding light on the contributions of microorganisms to One Health.

Mitigating climate change in soil ecosystems involves complex plant and microbial processes regulating carbon pools and flows. Here, we advocate for the use of soil microbiome interventions to help increase soil carbon stocks and curb greenhouse gas emissions from managed soils. Direct interventions include the introduction of microbial strains, consortia, phage, and soil transplants, whereas indirect interventions include managing soil conditions or additives to modulate community composition or its activities. Approaches to increase soil carbon stocks using microbially catalyzed processes include increasing carbon inputs from plants, promoting soil organic matter (SOM) formation, and reducing SOM turnover and production of diverse greenhouse gases. Marginal or degraded soils may provide the greatest opportunities for enhancing global soil carbon stocks. Among the many knowledge gaps in this field, crucial gaps include the processes influencing the transformation of plant-derived soil carbon inputs into SOM and the identity of the microbes and microbial activities impacting this transformation. As a critical step forward, we encourage broadening the current widespread screening of potentially beneficial soil microorganisms to encompass functions relevant to stimulating soil carbon stocks. Moreover, in developing these interventions, we must consider the potential ecological ramifications and uncertainties, such as incurred by the widespread introduction of homogenous inoculants and consortia, and the need for site-specificity given the extreme variation among soil habitats. Incentivization and implementation at large spatial scales could effectively harness increases in soil carbon stocks, helping to mitigate the impacts of climate change.

A good quality egg is essential for a successful pregnancy and early embryo development. Oocyte development is vulnerable to environmental exposures. Bisphenol S (BPS) is widely used as a replacement for its analog bisphenol A, but the reproductive toxicity of BPS has been of great concern. In this study, we showed that BPS exposure induces dysbiosis of the gut microbiota, which further leads to intestinal permeability and inflammation, and ultimately impairs oocyte quality. More importantly, we found that alginate oligosaccharide reshapes the gut microbiota to improve gut homeostasis, thereby preventing the deleterious effects of BPS on the gut and oocytes. Overall, this study not only demonstrates that BPS exposure impairs the intestine and oocytes by inducing dysbiosis of the gut microbiota but also develops a preventive strategy.

Importance: Oocyte development is vulnerable to stimulation by intrinsic and extrinsic factors, particularly many environmental pollutants and chemicals in daily life. The reproductive toxicity of bisphenol S has been of great concern, although it is widely used as a safe substitute for its analog bisphenol A. However, it is not known how bisphenol S impairs oocyte quality. This work presents the exciting finding that bisphenol S induces gut microbiota dysbiosis, which further leads to increased intestinal permeability and inflammation and ultimately damages oocytes. More importantly, we show that alginate oligosaccharide improves gut homeostasis by reshaping the gut microbiota, therefore preventing the bisphenol S-induced gut microbiota dysbiosis and gut and oocyte damage. These findings present a major advance in the understanding of bisphenol S toxicity to oocytes and also provide a preventive strategy.

Periodontitis is closely related to renal health, but the specific influence of Porphyromonas gingivalis (P. gingivalis), a key pathogen in periodontitis, on the development of acute kidney injury (AKI) in mice has not been fully elucidated. In our study, AKI was induced in mice through ischemia-reperfusion injury while administering oral infection with P. gingivalis. Comprehensive analyses were conducted, including 16S rRNA sequencing, liquid chromatography-mass spectrometry (LC-MS) metabolomics, and transcriptome sequencing. In vitro, the identified metabolite was used to stimulate mouse neutrophils. Subsequently, these modified neutrophils were co-cultured with mouse renal tubular epithelial cells. The results showed that oral infection with P. gingivalis significantly exacerbated AKI in mice. 16S rRNA sequencing revealed notable shifts in gut microbiota composition. LC-MS metabolomics analysis identified significant metabolic alterations, particularly the upregulation of 3-indoleacrylic acid in the serum. Transcriptome sequencing showed an increased expression of neutrophilic granule protein (Ngp), which was closely associated with 3-indoleacrylic acid, and the presence of Porphyromonas. Cellular experiments demonstrated that 3-indoleacrylic acid could activate neutrophils, leading to an elevation in NGP protein levels, a response that was associated with renal epithelial cell injury. Oral infection with P. gingivalis exacerbated AKI through the gut-kidney axis, involving gut microbiota dysbiosis, metabolic disturbances, and increased renal expression of Ngp.

Importance: This study provides novel insights into the relationship between periodontal health and renal function. Porphyromonas gingivalis oral infection disrupted the balance of gut microbiota and was an important modifier determining the severity of acute kidney injury. Under the "gut-kidney axis," P. gingivalis might cause an increase in the level of the gut microbial metabolite 3-indoleacrylic acid, interfering with kidney immunity and disrupting the maintenance of kidney epithelium.

The continuous interaction between phages and their respective hosts has resulted in the evolution of multiple bacterial immune mechanisms. However, the diversity and prevalence of antiviral defense systems in complex communities are still unknown. We therefore investigated the diversity and abundance of viral defense systems in 3,038 high-quality bacterial and archaeal genomes from the rumen. In total, 14,241 defense systems and 31,948 antiviral-related genes were identified. Those genes represented 114 unique system types grouped into 49 families. We observed a high prevalence of defense systems in the genomes. However, the number of defense systems, defense system families, and system density varied widely from genome to genome. Additionally, the number of defense system per genome correlated positively with the number of defense system families and the genome size. Restriction modification, Abi, and cas system families were the most common, but many rare systems were present in only 1% of the genomes. Antiviral defense systems are prevalent and diverse in the rumen, but only a few are dominant, indicating that most systems are rarely present. However, the collection of systems throughout the rumen may represent a pool of mechanisms that can be shared by different members of the community and modulate the phage-host interaction.IMPORTANCEPhages may act antagonistically at the cell level but have a mutualistic interaction at the microbiome level. This interaction shapes the structure of microbial communities and is mainly driven by the defense mechanism. However, the diversity of such mechanism is larger than previously thought. Because of that, we described the abundance and diversity of the antiviral defense system of a collection of genomes, metagenome-assembled genomes (MAGs) and isolates, from the rumen. While defense mechanisms seem to be prevalent among bacteria and archaea, only a few were common. This suggests that most of these defense mechanisms are not present in many rumen microbes but could be shared among different members of the microbial community. This is consistent with the "pan-immune system" model, which appears to be common across different environments.

The surveillance of mobile genetic elements facilitating the spread of antimicrobial resistance genes has been challenging. Here, we tracked both clonal and plasmid transmission in colistin- and carbapenem-resistant Klebsiella pneumoniae using short- and long-read sequencing technologies. We observed three clonal transmissions, all containing Incompatibility group (Inc) L plasmids and New Delhi metallo-beta-lactamase bla_NDM-1, although not co-located on the same plasmid. One IncL-bla_NDM-1 plasmid had been transferred between sequence type (ST) 392 and ST15, and the promiscuous IncL-bla_OXA-48 plasmid was likely shared between a singleton and a clonal transmission of ST392. Plasmids within clonal outbreaks and between clusters and STs had 0-2 single nucleotide polymorphism (SNP) differences, showing high stability upon transfer to same or different STs. The simplest explanation, without a comprehensive analysis with long-read sequencing, would be the spread of a single common IncL-bla_NDM-1 plasmid. However, here, we report bla_NDM-1 in five different plasmids, emphasizing the need to investigate plasmid-mediated transmission for effective containment of outbreaks.IMPORTANCEAntimicrobial resistance occupies a central stage in global public health emergencies. Recently, efforts to track the genetic elements that facilitate the spread of resistance genes in plasmids outbreaks, utilizing short-read sequencing technologies, have been described. However, incomplete plasmid reconstruction from short-read sequencing data hinders full knowledge about plasmid structure, which makes the exploration very challenging. In this study, we used both short- and long-read sequencing in clinical Klebsiella pneumoniae from University Hospital Centre Zagreb, Croatia, which was resistant to both last-resort antibiotics colistin and carbapenem. Our results show complex transmission networks and sharing of plasmids, emphasizing multiple transmissions of plasmids harboring carbapenem and/or colistin resistance genes between and within K. pneumoniae clones. Only full-length sequencing plus a novel way of determining plasmid clusters resulted in the complete picture, showing how future active monitoring of plasmids as a vital tool for infection prevention and control could be implemented.