npj Biofilms and Microbiomes最新文献

Implant-associated infections (IAIs) arise from immune dysregulation and the resilience of bacterial biofilms, which create a permissive niche for persistent infection. Biofilms further suppress host immunity and impair repair. Advances in nanoengineered surfaces and multifunctional antimicrobial coatings, together with gas-releasing and stimulus-responsive nanoplatforms, offer effective non-antibiotic strategies to inhibit colonization, disrupt biofilms, and modulate local immunity. This review summarizes emerging immune-informed approaches for treating IAIs.

Large-scale, decentralized microbiome sampling surveys and citizen science initiatives often require periods of storage at ambient temperature, potentially altering sample composition during collection and transport. We developed a generalizable framework to quantify and model these biases using sourdough as a tractable fermentation system, with samples subjected to controlled storage conditions (4 °C, 17 °C, 30 °C, regularly sampled up to 28 days). Machine-learning models paired with multi-omics profiling-including microbiome, targeted and untargeted metabolome profiling, and cultivation-revealed temperature-dependent shifts in bacterial community structure and metabolic profiles, while fungal communities remained stable. Storage induced ecological restructuring, marked by reduced network modularity and increased centrality of dominant taxa at higher temperatures. Notably, storage duration and temperature were strongly encoded in the multi-omics data, with temperature exerting a more pronounced influence than time. 24 of the top 25 predictors of storage condition were metabolites, underscoring functional layers as both sensitive to and informative of environmental exposure. These findings demonstrate that even short-term ambient storage (<2 days) can substantially reshape microbiome, metabolome, and biochemical profiles, posing risks to data comparability in decentralized studies and emphasizing the need to recognize and address such biases. Critically, the high predictability of storage history offers a path toward bias detection and correction- particularly when standardized collection protocols are infeasible, as is common in decentralized sampling contexts. Our approach enables robust quantification and modeling of such storage effects across multi-omics datasets, unlocking more accurate interpretation of large-scale microbiome surveys.

The establishment of microbial biofilms, communities embedded in self-produced extracellular matrices, poses growing challenges for health and antimicrobial management. Understanding biofilm formation is crucial for developing control and eradication strategies. In response to environmental cues, planktonic bacteria adopt a sessile lifestyle, coordinating growth with matrix production. We monitored cellulose biofilm formation by Pseudomonas sp. IsoF in real time using single-step fluorescent stains. Live-tracking of polysaccharide synthesis revealed dynamic matrix arrangements shaping final biofilm structure. Cellulose determined substratum adherence, cell contacts, and colony patterning in IsoF. Biofilms formed in flow-cells and at air-liquid interfaces were remarkably similar in composition, progression, and architecture. Artificial elevation of intracellular c-di-GMP levels produced cellulose-dependent biofilms distinct from the wild type and induced a secondary exopolysaccharide. Our fluorescent probes provide real-time visualization of matrix development, enabling detailed analysis of biofilm architecture and regulation in standard laboratory conditions.

The composition of the vaginal microenvironment has significant implications for gynecologic and obstetric outcomes. Where a Lactobacillus-dominated microenvironment is considered optimal, a polymicrobial environment is associated with increased risk for female reproductive diseases. Recent work examined bacteria-derived extracellular vesicles (bEVs) as an important mode of microbe-host communication that may influence reproductive outcomes. However, in order to communicate with female reproductive tissues, bEVs must penetrate the protective cervicovaginal mucus barrier. We demonstrate increased diffusion of bEVs compared to whole bacteria. Additionally, we evaluate the uptake of bEVs by, and the resulting effects on, human vaginal epithelial, endometrial, and placental cells, highlighting potential mechanisms of action by which vaginal dysbiosis contributes to gynecologic and obstetric diseases. Taken together, our work demonstrates the ability of bEVs to mediate female reproductive outcomes and highlights their potential as therapeutic modalities for treating dysbiosis and dysbiosis-associated diseases in the female reproductive tract.

Although disrupted bile acid (BA) homeostasis is implicated in necrotizing enterocolitis (NEC), its role in NEC pathogenesis remains unclear. We revealed that secondary BA accumulation in the ileum with severe NEC induced Paneth cell (PC) loss via the activation of the intestinal farnesoid X receptor (FXR). Single-cell RNA sequencing (scRNA-seq) showed that high FXR expression was associated with the differentiation of intestinal stem cells (ISCs) in NEC. Mechanistically, intestinal FXR upregulation induced PC loss by inhibiting Wnt/planar cell polarity (PCP) signaling, which regulates ISC lineage priming toward PCs. Furthermore, disrupting the gut-liver axis by downregulating FGF receptor 4 (FGFR4) abrogated the suppression of the BA synthesis induced by elevated FXR levels in severe NEC, leading to improved outcomes, including a restored Firmicutes/Bacteroidetes ratio and a normalized butyrate concentration. Interestingly, FGFR4 inhibition restored the PC population in a butyrate-dependent manner. Our findings demonstrate that FXR regulated PC generation directly or indirectly via the gut-liver axis.

This study investigated the relationship between constipation and autism-related symptoms in children with autism spectrum disorder (ASD). Participants were assessed for gastrointestinal (GI) and autism-related symptoms and classified into constipated and non-constipated groups. The relationship was further explored via 16S rRNA sequencing and non-targeted metabolomics to identify underlying mechanisms. Results revealed that constipated ASD children exhibited more severe autism-related symptoms and alterations in four bacterial taxa-the phylum Bacteroidetes, the family Barnesiellaceae, and the genera Alistipes and Bilophila-plus 451 metabolites compared to non-constipated ASD children. Among the altered bacterial taxa, three-Bacteroidetes, Alistipes, and Bilophila-exacerbated the relationship between constipation and autism-related symptoms. Five metabolites derived from the above three taxa-chenodeoxycholic acid, palmitic acid, glutaric acid, arachidonic acid, and choline-were significantly associated with autism-related symptoms. Our multi-omics analysis reveals the exacerbating effect of constipation on autism-related symptoms in children with ASD.

Miscarriage, the loss of a pregnancy before viability, can be sporadic or recurrent. Emerging evidence links miscarriage to specific microbiota compositions within the female reproductive tract (FRT). This systematic review aims to synthesise evidence on the association between sporadic and recurrent miscarriage and FRT microbiota composition, as assessed using metataxonomic profiling approaches. A systematic analysis of the 43 included studies, sampling the vaginal, cervical and endometrial microbiota supported an association between reduced Lactobacillus abundance and miscarriage, making it a potential target for therapeutic intervention. However, consistent changes in alpha and beta diversity were not observed and there was a lack of reproducibility for other compositional changes. This review also highlighted concerns about the significant bias introduced due to methodological variations and emphasises the need for future standardisation of microbial sampling, sequencing, and reporting to allow accurate comparison of results and to reduce research waste.

Oral intake of probiotics has been shown to positively impact depression, anxiety, stress and cognition. Recently, an effort was made to more objectively assess their impact on brain structure and function. However, there has been no exhaustive systematic assessment of outcomes of these studies, nor the techniques utilised. Therefore, we performed a systematic review on randomised, placebo-controlled trials assessing the effects of oral probiotic interventions on brain health by imaging or electrophysiology techniques in human adults. Of 2307 articles screened, 26 articles comprising 19 studies, totalling 762 healthy subjects or patients with various diseases, were ultimately included. The quality of most studies was high. Overall, probiotic intake appears to modify resting state connectivity and activity, decrease involvement of several brain regions during negative emotional stimulation, and improve sleep quality. Several studies found correlations between brain outcomes and clinical symptom ratings, supporting the relevance of brain imaging and electrophysiology techniques in this field.

Emerging evidence suggests a role of microbiota in prostate cancer, yet this association remains poorly understood. This review systematically examines microbes from the skin, oral cavity, gut, urinary tract, and the prostate cancer microenvironment, summarizing how these communities affect prostate cancer initiation, progression, and therapeutic response. We highlight key molecular pathways and metabolic reprogramming events underlying host-microbiota interactions and outline current findings and knowledge gaps to guide microorganism-based therapeutic strategies.

The gut microbiota influences host metabolism, immunity, and organ physiology, making it an attractive therapeutic target. However, clinical probiotic trials often produce inconsistent results, reflecting context-dependent effects shaped by metabolic, ecological, dietary, and host-specific factors. We critically synthesized the literature on hyperoxaluria, a condition of elevated urinary oxalate associated with kidney stones and chronic kidney disease, as a mechanistically tractable model for probiotic development. We examined evidence from clinical studies, microbiome analyses, and mechanistic experiments to identify factors influencing efficacy, with a focus on Oxalobacter formigenes, a specialist oxalate-degrading anaerobe. Across trials, probiotic success depended less on dose, strain identity, or persistence, and more on the ecological context - particularly the baseline abundance of oxalate-degrading genes (oxc, frc) in the native microbiota. Efficacy was highest when these metabolic niches were vacant. Diet, delivery format, and broader microbial community structure also shaped outcomes. A taxon-centric approach is insufficient for predicting probiotic efficacy. We propose a three-phase framework for rational design: (1) case-control microbiome studies to identify metabolically relevant deficits; (2) mechanistic in vivo and in vitro validation to establish causality; and (3) complex systems modeling to predict context-specific responses. This metabolism-first, ecology-grounded strategy is generalizable to other microbiota-linked conditions and supports precision microbial therapeutics.