npj Biofilms and Microbiomes最新文献

Gut microbiota members from the Bacteroidota phylum play a pivotal role in mammalian health and metabolism. They thrive in this diverse ecosystem due to their notable ability to cope with distinct recalcitrant dietary glycans via polysaccharide utilization loci (PULs). Our study reveals that a PUL from an herbivore gut bacterium belonging to the Bacteroidota phylum, with a gene composition similar to that in the human gut, exhibits extended functionality. While the human gut PUL targets mixed-linkage β-glucans specifically, the herbivore gut PUL also efficiently processes linear and substituted β-1,3-glucans. This gain of function emerges from molecular adaptations in recognition proteins and carbohydrate-active enzymes, including a β-glucosidase specialized for β(1,6)-glucosyl linkages, a typical substitution in β(1,3)-glucans. These findings broaden the existing model for non-cellulosic β-glucans utilization by gut bacteria, revealing an additional layer of functional and evolutionary complexity within the gut microbiota, beyond conventional gene insertions/deletions to intricate biochemical interactions.

Gynecologic cancers develop from the female reproductive organs. Microbial dysbiosis in the gut and oral cavity can communicate with each other through various ways, leading to mucosal destruction, inflammatory response, genomic instability, and ultimately inducing cancer and worsening. Here, we introduce the mechanisms of interactions between gut and oral microbiota and their changes in the development of gynecologic tumors. In addition, new therapeutic approaches based on microbiota modulation are discussed.

DNA is the genetic code found inside all living cells and its molecular stability can also be utilized outside the cell. While extracellular DNA (eDNA) has been identified as a structural polymer in bacterial biofilms, whether it persists stably throughout development remains unclear. Here, we report that eDNA is temporarily invested in the biofilm matrix before being reclaimed later in development. Specifically, by imaging eDNA dynamics within undomesticated Bacillus subtilis biofilms, we found eDNA is produced during biofilm establishment before being globally degraded in a spatiotemporally coordinated pulse. We identified YhcR, a secreted Ca²⁺-dependent nuclease, as responsible for eDNA degradation in pellicle biofilms. YhcR cooperates with two other nucleases, NucA and NucB, to reclaim eDNA for its phosphate content in colony biofilms. Our results identify extracellular nucleases that are crucial for eDNA reclamation during biofilm development and we therefore propose a new role for eDNA as a dynamic metabolic reservoir.

Understanding how Legionella spp. proliferate in multispecies biofilms is essential to develop strategies to control their presence in building plumbing. Here, we analyzed biofilm formation and Legionella spp. colonization on new plumbing material during 8 weeks. Biofilm formation was characterized by an initial increase in intact cell concentrations up to 9.5 × 10⁵ cells/cm², followed by a steady decrease. We identified Comamonas, Caulobacter, Schlegella, Blastomonas and Methyloversatilis as pioneer genera in the biofilm formation process. Importantly, L. pneumophila was the dominant Legionella spp. and rapidly colonized the biofilms, with culturable cell concentrations peaking at 3.1 × 10⁴ MPN/cm² after 4 weeks already. Moreover, several Legionella species co-occurred and had distinct dynamics of biofilm colonization. Vermamoeba vermiformis (V. vermiformis) was the dominant protist identified with 18S rRNA gene amplicon sequencing. Together our results highlight that biofilm formation upon introduction of new building plumbing material is a dynamic process where pathogenic Legionella species can be part of the earliest colonizers.

The Staphylococcus aureus (S. aureus) SaeRS two-component system (TCS) regulates over 20 virulence factors. While its impact on chronic infection has been thoroughly discussed, its role in the early stage of infection remains elusive. Since macrophages serve as the primary immune defenders at the onset of infection, this study investigates the influence of SaeRS on macrophage functions and elucidates the underlying mechanisms. Macrophage expression of inflammatory and chemotactic factors, phagocytosis, and bactericidal activity against S. aureus were assessed, along with the evaluation of cellular oxidative stress. SaeRS was found to impair macrophage function. Mechanistically, SaeRS inhibited NF-κB pathway activation via toll-like receptor 2 (TLR2). Its immune-modulating effect could partially be explained by the strengthened biofilm formation. More importantly, we found SaeRS compromised macrophage immune functions at early infection stages even prior to biofilm formation. These early immune evasion effects were dependent on bacterial clumping as cytokine secretion, phagocytosis, and bactericidal activity were repaired when clumping was inhibited. We speculate that the bacterial clumping-mediated antigen mask is responsible for SaeRS-mediated immune evasion at the early infection stage. In vivo, ΔsaeRS infection was cleared earlier, accompanied by early pro-inflammatory cytokines production, and increased tissue oxidative stress. Subsequently, macrophages transitioned to an anti-inflammatory state, thereby promoting tissue repair. In summary, our findings underscore the critical role of the SaeRS TCS in S. aureus pathogenicity, particularly during early infection, which is likely initiated by SaeRS-mediated bacterial clumping.

Due to unique genomic adaptations, Methanococcus maripaludis Mic1c10 is highly corrosive when in direct contact with Fe⁰. A critical adaptation involves increased glycosylation of an extracellular [NiFe]-hydrogenase, facilitating its anchoring to cell surface proteins. Corrosive strains adapt to the constructed environment via horizontal gene transfer while retaining ancestral genes important for intraspecies competition and surface attachment. This calls for a reevaluation of how the built environment impacts methane cycling.

Extracellular polysaccharides are crucial components for biofilm development. Although Bacillus subtilis is one of the most characterized Gram-positive biofilm model system, the structure-function of its exopolysaccharide, EpsA-O, remains to be elucidated. By combining chemical analysis, NMR spectroscopy, rheology, and molecular modeling, high-resolution data of EpsA-O structure from atom to supramolecular scale was obtained. The repeating unit is composed of the trisaccharide backbone [→3)-β-D-QuipNAc4NAc-(1→3)-β-D-GalpNAc-(1→3)-α-D-GlcpNAc-(1]_n, and the side chain β-D-Galp(3,4-S-Pyr)-(1→6)-β-D-Galp(3,4-S-Pyr)-(1→6)-α-D-Galp-(1→ linked to C4 of GalNAc. Close agreement between the primary structure and rheological behavior allowed us to model EpsA-O macromolecular and supramolecular solution structure, which can span the intercellular space forming a gel that leads to a complex 3D biofilm network as corroborated by a mutant strain with impaired ability to produce EpsA-O. This is a comprehensive structure-function investigation of the essential biofilm adhesive exopolysaccharide that will serve as a useful guide for future studies in biofilm architecture formation.

Ingestible microdevices represent a breakthrough in non-invasive sampling of the human gastrointestinal (GI) tract. By capturing the native spatiotemporal microbiome and intricate biochemical gradients, these devices allow a non-invasive multi-omic access to the unperturbed host-microbiota crosstalk, immune/nutritional landscapes and gut-organ connections. We present the current progress of GI sampling microdevices towards personalized metabolism and fostering collaboration among clinicians, engineers, and data scientists.

The gut microbiome plays a major role in human health; however, little is known about the structural arrangement of microbes and factors governing their distribution. In this work, we present an in silico agent-based model (ABM) to conceptually simulate the dynamics of gut mucosal bacterial communities. We explored how various types of metabolic interactions, including competition, neutralism, commensalism, and mutualism, affect community structure, through nutrient consumption and metabolite exchange. Results showed that, across scenarios with different initial species abundances, cross-feeding promotes species coexistence. Morphologically, competition and neutralism resulted in segregation, while mutualism and commensalism fostered high intermixing. In addition, cooperative relations resulted in community properties with little sensitivity to the selective uptake of metabolites produced by the host. Moreover, metabolic interactions strongly influenced colonization success following the invasion of newcomer species. These results provide important insights into the utility of ABM in deciphering complex microbiome patterns.

The gut microbiome has been implicated in various human diseases, though findings across studies have shown considerable variability. In this study, we reanalyzed 6314 publicly available fecal metagenomes from 36 case-control studies on different diseases to investigate microbial diversity and disease-shared signatures. Using a unified analysis pipeline, we observed reduced microbial diversity in many diseases, while some exhibited increased diversity. Significant alterations in microbial communities were detected across most diseases. A meta-analysis identified 277 disease-associated gut species, including numerous opportunistic pathogens enriched in patients and a depletion of beneficial microbes. A random forest classifier based on these signatures achieved high accuracy in distinguishing diseased individuals from controls (AUC = 0.776) and high-risk patients from controls (AUC = 0.825), and it also performed well in external cohorts. These results offer insights into the gut microbiome's role in common diseases in the Chinese population and will guide personalized disease management strategies.