Nat Commun. 2025 Mar 21;16(1):2223. doi: 10.1038/s41467-025-57345-0.

ABSTRACT

The delay between the origin of animals in the Neoproterozoic and their Cambrian diversification remains perplexing. Animal diversification mirrors an expansion in marine shelf area under a greenhouse climate, though the extent to which these environmental conditions directly influenced physiology and early organismal ecology remains unclear. Here, we use a biogeochemical model to quantify oxygen dynamics at the sunlit sediment-water interface over day-night (diel) cycles at warm and cold conditions. We find that warm temperatures dictated physiologically stressful diel benthic oxic-anoxic shifts over a nutrient-rich shelf. Under these conditions, a population-and-phenotype model further show that the benefits of efficient cellular oxygen sensing that can offer adaptations to stress outweigh its cost. Since diurnal benthic redox variability would have expanded as continents were flooded in the end-Neoproterozoic and early Palaeozoic, we propose that a combination of physiological stress and ample resources in the benthic environment may have impacted the adaptive radiation of animals tolerant to oxygen fluctuations.

PMID:40118825 | DOI:10.1038/s41467-025-57345-0

Neurotherapeutics. 2025 Mar 20:e00575. doi: 10.1016/j.neurot.2025.e00575. Online ahead of print.

ABSTRACT

Neuroblastoma is an aggressive childhood cancer that arises from the sympathetic nervous system. Despite advances in treatment, high-risk neuroblastoma remains difficult to manage due to its heterogeneous nature and frequent development of drug resistance. Drug repurposing guided by single-cell analysis presents a promising strategy for identifying new therapeutic options. Here, we aim to characterize high-risk neuroblastoma subpopulations and identify effective repurposed drugs for targeted treatment. We performed single-cell transcriptomic analysis of neuroblastoma samples, integrating bulk RNA-seq data deconvolution with clinical outcomes to define distinct malignant cell states. Using a systematic drug repurposing pipeline, we identified and validated potential therapeutic agents targeting specific high-risk neuroblastoma subpopulations. Single-cell analysis revealed 17 transcriptionally distinct neuroblastoma subpopulations. Survival analysis identified a highly aggressive subpopulation characterized by elevated UBE2C/PTTG1 expression and poor patient outcomes, distinct from a less aggressive subpopulation with favorable prognosis. Drug repurposing screening identified Adavosertib as particularly effective against the aggressive subpopulation, validated using SK-N-DZ cells as a representative model. Mechanistically, Adavosertib suppressed cell proliferation through AKT/mTOR pathway disruption, induced G2/M phase cell cycle arrest, and promoted apoptosis. Further analysis revealed UBE2C and PTTG1 as key molecular drivers of drug resistance, where their overexpression enhanced proliferation, Adavosertib resistance, and cell migration. This study establishes a single-cell-based drug repurposing strategy for high-risk neuroblastoma treatment. Our approach successfully identified Adavosertib as a promising repurposed therapeutic agent for targeting specific high-risk neuroblastoma subpopulations, providing a framework for developing more effective personalized treatment strategies.

PMID:40118716 | DOI:10.1016/j.neurot.2025.e00575

Med Mycol. 2025 Mar 21:myaf025. doi: 10.1093/mmy/myaf025. Online ahead of print.

ABSTRACT

Candida albicans is a major human fungal pathogen; however, limited antifungal agents, undesirable drug side effects, and ineffective prevention of drug-resistant strains have become serious problems. Chitosan is a nontoxic, biodegradable, and biocompatible linear polysaccharide made from the deacetylation of chitin. In this study, a ZCF31 putative transcription factor gene was selected from a previous mutant library screen, as zcf31Δ strains exhibited defective cell growth in response to chitosan. Furthermore, chitosan caused notable damage to zcf31Δ cells; however, ZCF31 expression was not significantly changed by chitosan, suggesting that zcf31Δ is sensitive to chitosan could be due to changes in the physical properties of C. albicans. Indeed, zcf31Δ cells displayed significant increases in cell wall thickness. Consistent to the previous study, zcf31Δ strains were resistant to calcofluor white but highly susceptible to SDS. These results implied that chitosan mainly influences membrane function, as zcf31Δ strengthens the stress resistance of the fungal cell wall but lessens cell membrane function. Interestingly, this effect on the cell surface mechanics of the C. albicans zcf31Δ strains was not responsible for the virulence-associated function. RNA-seq analysis further revealed that six mannosyltransferase-related genes were upregulated in zcf31Δ. Although five mannosyltransferase-related mutant strains in the zcf31Δ background partially reduced the cell wall thickness, only zcf31Δ/mnn45Δ showed the recovery of chitosan resistance. Our findings suggest that Zcf31 mediates a delicate and complicated dynamic balance between the cell membrane and cell wall architectures through the mannosyltransferase genes in C. albicans, leading to altered chitosan susceptibility.

PMID:40118513 | DOI:10.1093/mmy/myaf025

Cell Syst. 2025 Mar 17:101239. doi: 10.1016/j.cels.2025.101239. Online ahead of print.

ABSTRACT

A major contributor to poor sensitivity to anti-cancer kinase inhibitor therapy is drug-induced cellular adaptation, whereby remodeling of signaling and gene regulatory networks permits a drug-tolerant phenotype. Here, we resolve the scale and kinetics of critical subcellular events following oncogenic kinase inhibition and preceding cell cycle re-entry, using mass spectrometry-based phosphoproteomics and RNA sequencing (RNA-seq) to monitor the dynamics of thousands of growth- and survival-related signals over the first minutes, hours, and days of oncogenic BRAF inhibition in human melanoma cells. We observed sustained inhibition of the BRAF-ERK axis, gradual downregulation of cell cycle signaling, and three distinct, reversible phase transitions toward quiescence. Statistical inference of kinetically defined regulatory modules revealed a dominant compensatory induction of SRC family kinase (SFK) signaling, promoted in part by excess reactive oxygen species, rendering cells sensitive to co-treatment with an SFK inhibitor in vitro and in vivo, underscoring the translational potential for assessing early drug-induced adaptive signaling. A record of this paper's transparent peer review process is included in the supplemental information.

PMID:40118060 | DOI:10.1016/j.cels.2025.101239

Elife. 2025 Mar 21;14:RP102019. doi: 10.7554/eLife.102019.

ABSTRACT

The mammalian suprachiasmatic nucleus (SCN), situated in the ventral hypothalamus, directs daily cellular and physiological rhythms across the body. The SCN clockwork is a self-sustaining transcriptional-translational feedback loop (TTFL) that in turn coordinates the expression of clock-controlled genes (CCGs) directing circadian programmes of SCN cellular activity. In the mouse, the transcription factor, ZFHX3 (zinc finger homeobox-3), is necessary for the development of the SCN and influences circadian behaviour in the adult. The molecular mechanisms by which ZFHX3 affects the SCN at transcriptomic and genomic levels are, however, poorly defined. Here, we used chromatin immunoprecipitation sequencing to map the genomic localization of ZFHX3-binding sites in SCN chromatin. To test for function, we then conducted comprehensive RNA sequencing at six distinct times-of-day to compare the SCN transcriptional profiles of control and ZFHX3-conditional null mutants. We show that the genome-wide occupancy of ZFHX3 occurs predominantly around gene transcription start sites, co-localizing with known histone modifications, and preferentially partnering with clock transcription factors (CLOCK, BMAL1) to regulate clock gene(s) transcription. Correspondingly, we show that the conditional loss of ZFHX3 in the adult has a dramatic effect on the SCN transcriptome, including changes in the levels of transcripts encoding elements of numerous neuropeptide neurotransmitter systems while attenuating the daily oscillation of the clock TF Bmal1. Furthermore, various TTFL genes and CCGs exhibited altered circadian expression profiles, consistent with an advanced in daily behavioural rhythms under 12 h light-12 h dark conditions. Together, these findings reveal the extensive genome-wide regulation mediated by ZFHX3 in the central clock that orchestrates daily timekeeping in mammals.

PMID:40117332 | DOI:10.7554/eLife.102019

Database (Oxford). 2025 Mar 21;2025:baaf020. doi: 10.1093/database/baaf020.

ABSTRACT

Ontologies are widely used in databases to standardize data, improving data quality, integration, and ease of comparison. Within ontologies tailored to diverse use cases, post-composing user-defined terms reconciles the demands for standardization on the one hand and flexibility on the other. In many instances of Breedbase, a digital ecosystem for plant breeding designed for genomic selection, the goal is to capture phenotypic data using highly curated and rigorous crop ontologies, while adapting to the specific requirements of plant breeders to record data quickly and efficiently. For example, post-composing enables users to tailor ontology terms to suit specific and granular use cases such as repeated measurements on different plant parts and special sample preparation techniques. To achieve this, we have implemented a post-composing tool based on orthogonal ontologies providing users with the ability to introduce additional levels of phenotyping granularity tailored to unique experimental designs. Post-composed terms are designed to be reused by all breeding programs within a Breedbase instance but are not exported to the crop reference ontologies. Breedbase users can post-compose terms across various categories, such as plant anatomy, treatments, temporal events, and breeding cycles, and, as a result, generate highly specific terms for more accurate phenotyping.

PMID:40117331 | DOI:10.1093/database/baaf020

Stem Cell Rev Rep. 2025 Mar 21. doi: 10.1007/s12015-025-10867-y. Online ahead of print.

NO ABSTRACT

PMID:40117085 | DOI:10.1007/s12015-025-10867-y

Mycorrhiza. 2025 Mar 21;35(2):24. doi: 10.1007/s00572-025-01191-x.

ABSTRACT

Some heavy metal tolerant fungal isolates capable of forming ericoid mycorrhiza can also confer increased metal tolerance to the host plant. One of these fungal isolates, Oidiodendron maius Zn, has been characterized and a few molecular mechanisms underlying its metal tolerant phenotype have been identified. Here, we investigate the genomic divergences between the available genome of O. maius Zn and the genomes of metal tolerant and sensitive isolates of O. maius, with the aim of identifying genes or intergenic regions possibly involved in the display of the tolerance. The resequenced genomes of 8 tolerant and 10 sensitive isolates were mapped on the reference, O. maius Zn, yielding 357 gene models from the reference that were either missing or too polymorphic to be identified in the genomes of the sensitive isolates. These regions included genes with functions related to defense mechanisms and with unknown functions. One third of the predicted gene models turned out to be highly polymorphic, including many enriched GO terms, i.e. DNA/RNA metabolism and modification, chromosome/chromatin organization, protein biosynthesis, metabolism and function, energy consumption/transfer and mitochondrion. Overall, our findings indicate that the tolerant phenotype in O. maius likely arises from multiple genetic adaptations rather than a singular mechanism.

PMID:40116937 | DOI:10.1007/s00572-025-01191-x

JMIR Rehabil Assist Technol. 2025 Mar 21;12:e60162. doi: 10.2196/60162.

ABSTRACT

BACKGROUND: Knee osteoarthritis (OA) is a common chronic condition that impairs mobility and diminishes quality of life. Despite the proven benefits of exercise therapy and patient education in managing OA pain and functional limitations, these strategies are often underused. To motivate and enhance patient engagement, personalized outcome prediction models can be used. However, the accuracy of existing models in predicting changes in knee pain outcomes remains insufficiently examined.

OBJECTIVE: This study aims to validate existing models and introduce a concise personalized model predicting changes in knee pain from before to after participating in a supervised patient education and exercise therapy program (GLA:D) among patients with knee OA.

METHODS: Our prediction models leverage self-reported patient information and functional measures. To refine the number of variables, we evaluated the variable importance and applied clinical reasoning. We trained random forest regression models and compared the rate of true predictions of our models with those using average values. In supplementary analyses, we additionally considered recently added variables to the GLA:D registry.

RESULTS: We evaluated the performance of a full, continuous, and concise model including all 34 variables, all 11 continuous variables, and the 6 most predictive variables, respectively. All three models performed similarly and were comparable to the existing model, with R2 values of 0.31-0.32 and root-mean-squared errors of 18.65-18.85-despite our increased sample size. Allowing a deviation of 15 (visual analog scale) points from the true change in pain, our concise model correctly estimated the change in pain in 58% of cases, while using average values that resulted in 51% accuracy. Our supplementary analysis led to similar outcomes.

CONCLUSIONS: Our concise personalized prediction model provides more often accurate predictions for changes in knee pain after the GLA:D program than using average pain improvement values. Neither the increase in sample size nor the inclusion of additional variables improved previous models. Based on current knowledge and available data, no better predictions are possible. Guidance is needed on when a model's performance is good enough for clinical practice use.

PMID:40116731 | DOI:10.2196/60162

Brief Bioinform. 2025 Mar 4;26(2):bbaf110. doi: 10.1093/bib/bbaf110.

ABSTRACT

As multi-omics sequencing technologies advance, the need for simulation tools capable of generating realistic and diverse (bulk and single-cell) multi-omics datasets for method testing and benchmarking becomes increasingly important. We present MOSim, an R package that simulates both bulk (via mosim function) and single-cell (via sc_mosim function) multi-omics data. The mosim function generates bulk transcriptomics data (RNA-seq) and additional regulatory omics layers (ATAC-seq, miRNA-seq, ChIP-seq, Methyl-seq, and transcription factors), while sc_mosim simulates single-cell transcriptomics data (scRNA-seq) with scATAC-seq and transcription factors as regulatory layers. The tool supports various experimental designs, including simulation of gene co-expression patterns, biological replicates, and differential expression between conditions. MOSim enables users to generate quantification matrices for each simulated omics data type, capturing the heterogeneity and complexity of bulk and single-cell multi-omics datasets. Furthermore, MOSim provides differentially abundant features within each omics layer and elucidates the active regulatory relationships between regulatory omics and gene expression data at both bulk and single-cell levels. By leveraging MOSim, researchers will be able to generate realistic and customizable bulk and single-cell multi-omics datasets to benchmark and validate analytical methods specifically designed for the integrative analysis of diverse regulatory omics data.

PMID:40116657 | DOI:10.1093/bib/bbaf110

New Phytol. 2025 Mar 21. doi: 10.1111/nph.70095. Online ahead of print.

ABSTRACT

Whole-genome duplications, widely observed in plant lineages, have significant evolutionary and ecological impacts. Yet, our current understanding of the direct implications of ploidy shifts on short- and long-term plant evolution remains fragmentary, necessitating further investigations across multiple ploidy levels. Chlamydomonas reinhardtii is a valuable model organism with profound potential to study the impact of ploidy increase on the longer term in a laboratory environment. This is partly due to the ability to increase the ploidy level. We developed a strategy to engineer ploidy in C. reinhardtii using noninterfering, antibiotic, selectable markers. This approach allows us to induce higher ploidy levels in C. reinhardtii and is applicable to field isolates, which expands beyond specific auxotroph laboratory strains and broadens the genetic diversity of parental haploid strains that can be crossed. We implement flow cytometry for precise measurement of the genome size of strains of different ploidy. We demonstrate the creation of diploids, triploids, and tetraploids by engineering North American field isolates, broadening the application of synthetic biology principles in C. reinhardtii. However, our newly formed triploids and tetraploids show signs of rapid aneuploidization. Our study greatly facilitates the application of C. reinhardtii to study polyploidy, in both fundamental and applied settings.

PMID:40116553 | DOI:10.1111/nph.70095

mSystems. 2025 Mar 21:e0140724. doi: 10.1128/msystems.01407-24. Online ahead of print.

ABSTRACT

Cobamides, the vitamin B12 (cobalamin) family of cofactors, are used by most organisms but produced by only a fraction of prokaryotes, and are thus considered key shared nutrients among microbes. Cobamides are structurally diverse, with multiple different cobamides found in most microbial communities. The ability to use different cobamides has been tested for several bacteria and microalgae, and nearly all show preferences for certain cobamides. This approach is limited by the commercial unavailability of cobamides other than cobalamin. Here, we have extracted and purified seven commercially unavailable cobamides to characterize bacterial cobamide preferences based on growth in specific cobamide-dependent conditions. The tested bacteria include engineered strains of Escherichia coli, Sinorhizobium meliloti, and Bacillus subtilis expressing native or heterologous cobamide-dependent enzymes, cultured under conditions that functionally isolate specific cobamide-dependent processes such as methionine synthesis. Comparison of these results to those of previous studies of diverse bacteria and microalgae revealed that a broad diversity of cobamide preferences exists not only across different organisms but also between different cobamide-dependent metabolic pathways within the same organism. The microbes differed in the cobamides that support growth most efficiently, cobamides that do not support growth, and the minimum cobamide concentrations required for growth. The latter differ by up to four orders of magnitude across organisms from different environments and by up to 20-fold between cobamide-dependent enzymes within the same organism. Given that cobamides are shared, required for use of specific growth substrates, and essential for central metabolism in certain organisms, cobamide preferences likely impact community structure and function.IMPORTANCENearly all bacteria are found in microbial communities with tens to thousands of other species. Molecular interactions such as metabolic cooperation and competition are key factors underlying community assembly and structure. Cobamides, the vitamin B12 family of enzyme cofactors, are one such class of nutrients, produced by only a minority of prokaryotes but required by most microbes. A unique aspect of cobamides is their broad diversity, with nearly 20 structural forms identified in nature. Importantly, this structural diversity impacts growth as most bacteria that have been tested show preferences for specific cobamide forms. We measured cobamide-dependent growth in several model bacteria and compared the results to those of previous analyses of cobamide preference. We found that cobamide preferences vary widely across bacteria, showing the importance of characterizing these aspects of cobamide biology to understand the impact of cobamides on microbial communities.

PMID:40116488 | DOI:10.1128/msystems.01407-24

Front Genet. 2025 Mar 6;16:1572670. doi: 10.3389/fgene.2025.1572670. eCollection 2025.

ABSTRACT

[This corrects the article DOI: 10.3389/fgene.2021.646297.].

PMID:40115817 | PMC:PMC11922946 | DOI:10.3389/fgene.2025.1572670

Front Mol Neurosci. 2025 Mar 6;18:1558715. doi: 10.3389/fnmol.2025.1558715. eCollection 2025.

NO ABSTRACT

PMID:40115378 | PMC:PMC11922866 | DOI:10.3389/fnmol.2025.1558715

Plant Cell Environ. 2025 Mar 20. doi: 10.1111/pce.15486. Online ahead of print.

ABSTRACT

Virus-induced gene silencing (VIGS) is an attractive reverse genetics tool for gene silencing in difficult to transform plants. Although a few VIGS vectors have been developed for soybean, they were never utilised for functional analysis of nodulation, a critical process for improving sustainable soybean cultivation. This is unfortunate, because several genes regulating this process are expressed in the upper parts of the plant, hence remain understudied due to limitations of the commonly used fast Agrobacterium rhizogenes-mediated hairy root transformation and stable transformation approaches. An instance involves components of the autoregulation of nodulation (AON) pathway controlling the optimal number of nodules through systemic long-distance root-shoot-root signalling pathway. We developed a fast and reliable VIGS protocol based on cowpea severe mosaic virus and used it to examine the roles a selected set of known AON genes in nodulation. We demonstrate the effectiveness of cowpea severe mosaic virus-based VIGS in silencing genes in below- and aboveground tissues and establish VIGS as a valuable tool to study nodulation in soybean.

PMID:40114323 | DOI:10.1111/pce.15486

EMBO Rep. 2025 Mar 20. doi: 10.1038/s44319-025-00426-4. Online ahead of print.

ABSTRACT

Plants utilize cell surface-localized pattern recognition receptors (PRRs) and intracellular nucleotide-binding leucine-rich repeat (NLR) receptors to detect non-self and elicit robust immune responses. Fine-tuning the homeostasis of these receptors is critical to prevent their hyperactivation. Here, we show that Arabidopsis plants lacking metacaspase 1 (AtMC1) display autoimmunity dependent on immune signalling components downstream of NLR and PRR activation. Overexpression of a catalytically inactive AtMC1 in an atmc1 background triggers severe autoimmunity partially dependent on the same immune signalling components. Overexpression of the E3 ligase SNIPER1, a master regulator of NLR homeostasis, fully reverts the AtMC1-dependent autoimmunity phenotype, inferring that a broad defect in NLR turnover may underlie the severe phenotype observed. Catalytically inactive AtMC1 localizes to punctate structures that are degraded through autophagy. Considering also previous evidence on the proteostatic functions of AtMC1, we speculate that Wt AtMC1 may either directly or indirectly control NLR protein levels, thereby preventing autoimmunity.

PMID:40113992 | DOI:10.1038/s44319-025-00426-4

Sci Rep. 2025 Mar 20;15(1):9668. doi: 10.1038/s41598-025-93377-8.

ABSTRACT

Disease classification is important for understanding disease commonalities on both the phenotypical and molecular levels. Based on predicted disease mode of action (MOA) proteins, our algorithm PICMOA (Pan-disease Classification in Mode of Action Protein Space) classifies 3526 diseases across 20 clinically classified classifications (ICD10-CM major classifications). At the top level, all diseases can be classified into "infectious" and "non-infectious" diseases. Non-infectious diseases are classified into 9 classes. To demonstrate the validity of the classifications, for common pathways predicted based on MOA proteins, 77% of the top 10 most frequent pathways have literature evidence of association to their respective disease classes/subclasses. These results indicate that PICMOA will be useful for understanding common disease mechanisms and facilitating the development of drugs for a class of diseases, rather than a single disease. The MOA proteins, molecular functions, pathways for classes, and individual diseases are available at https://sites.gatech.edu/cssb/PICMOA/ .

PMID:40113859 | DOI:10.1038/s41598-025-93377-8

Nat Commun. 2025 Mar 20;16(1):2770. doi: 10.1038/s41467-025-58076-y.

ABSTRACT

Inorganic phosphate (Pi) has essential metabolic and structural roles in living organisms. The Pi exporter, XPR1/SLC53A1, is critical for cellular Pi homeostasis. When intercellular Pi is high, cells accumulate inositol pyrophosphate (1,5-InsP8), a signaling molecule required for XPR1 function. Inactivating XPR1 mutations lead to brain calcifications, causing neurological symptoms including movement disorders, psychosis, and dementia. Here, cryo-electron microscopy structures of dimeric XPR1 and functional characterization delineate the substrate translocation pathway and how InsP8 initiates Pi transport. Binding of InsP8 to XPR1, but not the related inositol polyphosphate InsP6, rigidifies the intracellular SPX domains, with InsP8 bridging the dimers and SPX and transmembrane domains. Locked in this state, the C-terminal tail is sequestered, revealing the entrance to the transport pathway, thus explaining the obligate roles of the SPX domain and InsP8. Together, these findings advance our understanding of XPR1 transport activity and expand opportunities for rationalizing disease mechanisms and therapeutic intervention.

PMID:40113814 | DOI:10.1038/s41467-025-58076-y

ACS Nano. 2025 Mar 20. doi: 10.1021/acsnano.4c15538. Online ahead of print.

ABSTRACT

Bacterial microcompartments (BMCs) are proteinaceous organelles that self-assemble into selectively permeable shells that encapsulate enzymatic cargo. BMCs enhance catalytic pathways by reducing crosstalk among metabolites, preventing harmful intermediates from leaking into the cytosol and increasing reaction efficiency via enzyme colocalization. The intrinsic properties of BMCs make them attractive for biotechnological engineering. However, in vivo expression methods for shell synthesis have significant drawbacks that limit the potential design space for these nanocompartments. Here, we describe the development of an efficient and rapid method for the in vitro assembly of BMC shells from their protein building blocks. Our method enables large-scale construction of BMC shells by utilizing urea as a chaotropic agent to control self-assembly and provides an approach for encapsulation of both biotic and abiotic cargo under a broad range of reaction conditions. We demonstrate an enhanced level of control over the assembly of BMC shells in vitro and expand the design parameter space for engineering BMC systems with specialized and enhanced catalytic properties.

PMID:40113598 | DOI:10.1021/acsnano.4c15538

FEMS Microbiol Ecol. 2025 Mar 20:fiaf028. doi: 10.1093/femsec/fiaf028. Online ahead of print.

ABSTRACT

Environmental factors like diet and antibiotics modulate the gut microbiota in early life. During weaning, gut microbiota progressively diversifies through exposure to non-digestible carbohydrates (NDCs) from diet, while antibiotic perturbations might disrupt this process. Supplementing an infant's diet with prebiotic NDCs may mitigate the adverse effects of antibiotics on gut microbiota development. This study evaluated the influence of supplementation with 2-fucosyllactose (2'-FL), galacto-oligosaccharides (GOS), or isomalto/malto-polysaccharides containing 87% of α(1→6) linkages (IMMP-87), on the recovery of antibiotic-perturbed microbiota. The TIM-2 in vitro colon model inoculated with fecal microbiota of nine-month-old infants was used to simulate the colon of weaning infants exposed to the antibiotics amoxicillin/clavulanate or azithromycin. Both antibiotics induced changes in microbiota composition, with no signs of recovery in azithromycin-treated microbiota within 72 h. Moreover, antibiotic exposure affected microbiota activity, indicated by a low valerate production, and azithromycin treatment was associated with increased succinate production. The IMMP-87 supplementation promoted the compositional recovery of amoxicillin/clavulanate-perturbed microbiota, associated with the recovery of Ruminococcus, Ruminococcus gauvreauii group, and Holdemanella. NDC supplementation did not influence compositional recovery of azithromycin-treated microbiota. Irrespective of antibiotic exposure, supplementation with 2'-FL, GOS, or IMMP-87 enhanced microbiota activity by increasing short-chain fatty acids production (acetate, propionate, and butyrate).

PMID:40113239 | DOI:10.1093/femsec/fiaf028