Prebiotic potential of turmeric and fingerroot polysaccharides: modulation of human gut microbiota and metabolite profiles in in vitro colonic fermentation

Harnessing the power of microbiome, nanotechnology, and immunity against cancer.

Inference for stationary Log-Gaussian Cox point processes using Bayesian deep learning: Application to human oral microbiome image data

A global-scale framework for quantifying the gut microbiome's mediating role in environmental and personal determinants of health.

Biofilms formed by human skin microbiota on stainless steel surfaces: implications for pathogen control in food environments

Understanding the probiotic potential of a healthy human vaginal flora, Lactobacillus gasseri K9: genomic and in vitro aspects

The human microbiota comprises a vast and diverse array of microorganisms that play critical roles in maintaining health and modulating diseases. Engineered live biotherapeutic products (eLBPs) harness genetically modified microbes to perform defined therapeutic functions within the host. A central challenge in developing effective eLBPs is the rational selection of an appropriate microbial chassis, which requires consideration of safety, genetic tractability, functional performance and the target host niche. As different body sites present distinct physiological and biochemical conditions that influence microbial survival, colonisation and activity, choosing a chassis well-adapted to the target niche is essential for therapeutic durability and sustained efficacy. This review summarises microbial chassis that have been widely employed for the gut, skin, vagina and tumour microenvironment, highlighting how their characteristics enable effective function within these niches. Strategies to improve eLBP colonisation within these niches are discussed, and emerging microbial candidates that hold promise as future eLBPs are also identified.

The gut microbiome plays a crucial role in host homeostasis, with implications for nutrition, immune development, metabolism, and protection against pathogens. Disturbance of the microbiome by microbial invasion can be negative or positive: invasions of opportunistic pathogens can cause disease while dysbiotic states need invasions to recover. However, the complexity of the microbiome challenges our understanding of what factors determine the ability of microbes to invade. In this study, we measure interactions between members of a synthetic community of prominent gut bacteria using supernatant assays, which quantify the growth of one species in the cell-free culture medium of another. We measure relative abundances of co-cultures of up to four species to validate a generalized Lotka-Volterra model parameterized with these supernatant assays. We predict differential invasion outcomes of the opportunistic pathogens Escherichia coli and Bacteroides ovatus based on their monoculture growth profiles and interactions with other species, and we experimentally confirm model predictions of invasion success. The predictive value of our model indicates that environmentally mediated interactions, e.g., through soluble chemicals, primarily determine co-culture abundances and invasion success. Furthermore, model analyses show that negative interactions within the resident community and neutral to positive interactions with the invading species promote invasion success, but the interactions toward the invading species dominate. Our validated approach opens the way for testing of interactions of human gut microbiome species, thereby developing interventions to avoid pathogenic overgrowth and therapies to enhance health-benefitting invasions.IMPORTANCEThe stability of the human gut microbiome is crucial for host health, with opportunistic pathogen invasions causing diseases and healthy strain replacements needed for recovery. The microbiota's complexity complicates the understanding of invasion outcomes. This study uses a 10-species synthetic community of common gut microbiota to predict stable communities and invasion success. We grow cells in the growth medium of other species with the cells removed to parameterize a computational model, accurately predicting community composition up to four species and invasion success of Escherichia coli and Bacteroides ovatus. Our findings show that interactions through soluble compounds in the environment dictate co-culture growth and invasions. Furthermore, model analysis shows that interactions within the resident community and toward the invader are both important, but the latter dominate. These results pave the way for larger-scale studies to characterize gut microbiome interactions and properties that resist invasions, potentially benefiting health through improved probiotics and fecal microbiota transplants.

Antimicrobial resistance (AMR) poses a critical threat to global health, particularly in intensive care units, where vulnerable patients are frequently exposed to multidrug-resistant microorganisms. The human gut microbiome serves as a key reservoir for AMR genes, which can disseminate to other body sites, including the lungs, especially during severe illness. We applied Hi-C metagenomics to stool samples from 11 critically ill COVID-19 patients and analyzed microbial isolates from their lungs to investigate intra-host transmission of AMR genes. Plasmid-resolved microbial interaction networks revealed AMR gene sharing across 13 bacterial genera, primarily from Firmicutes and Proteobacteria, with evidence of plasmid-mediated transfer across phylum boundaries and between gut and lung compartments. Notably, we identified genetically identical Klebsiella pneumoniae strains colonizing both the gut and lungs of a single patient, as well as shared plasmids carrying qnrS-1 and blaCTX-M-231 resistance genes between gut Escherichia coli and lung K. pneumoniae. In addition to bacterial pathogens, Candida yeast species isolated from both niches harbored resistance genes to multiple antifungal classes, including azoles. These findings underscore the dynamic, cross-compartmental nature of AMR dissemination within the human body and highlight the importance of integrative surveillance strategies to control resistance in clinical settings.IMPORTANCEWhile COVID-19 itself caused severe illness, many deaths were ultimately due to secondary microbial infections-often worsened by antibiotic resistance. Plasmids, which shuttle resistance genes between bacterial species, are key players in their spread, yet their roles in transmission, especially across body sites such as the gut and lungs, are to be elucidated. The use of Hi-C metagenomics allowed us to map bacterium-plasmid links in the guts of severe COVID-19 patients and reconstruct high-quality genomes of opportunistic fungi. Comparing these with lung-derived isolate genomes, we gained insight into possible intra-host dissemination routes of resistance genes. Preparing for future pandemics will require not only rapid pathogen detection but also tools to monitor microbiome health and resistance dynamics, and understanding how treatments and microbial imbalances shape infection risks.

Classification of human gut microbiome into distinct enterotypes based on gut microbial community composition has provided an attractive framework for population stratification. While empirical evidence indicates that microbial enterotype is related to brain function and memory, the neural processes underlying this interaction remain to be further characterized. In 510 healthy young adults, we used 16S rDNA amplicon sequencing to perform enterotyping, acquired resting-state functional MRI data to calculate brain functional measures, and assessed both episodic and working memories. Inter-enterotype differences in brain functional measures were examined, followed by performance of correlation and mediation analyses to disentangle the potential associations between enterotype, brain function, and memory. We found significant differences in multiple brain functional measures in the parietal and occipital cortices across Bacteroides, Prevotella, and Ruminococcaceae enterotypes. Moreover, these differential brain functional measures were correlated with both episodic and working memories, and further mediated the relationship between enterotype and memory. Our findings not only establish brain function as the mediating factor between enterotype and memory, but also hold translational potential for informing novel treatment for cognitive dysfunction via targeting the microbiota-gut-brain axis.

Atherosclerosis is a chronic inflammatory disease influenced by host-microbiota interactions beyond traditional risk factors. Microbial communities in the oral cavity, gut, and blood contribute to vascular dysfunction through metabolic and immune mechanisms, yet an integrated perspective across these compartments remains lacking. This narrative review synthesizes current evidence on the distinct and interconnected roles of oral, gut, and blood microbiotas in atherosclerosis pathogenesis. We critically evaluate key microbial metabolites, trimethylamine N-oxide (TMAO), short-chain fatty acids (SCFAs), and secondary bile acids, and their mechanisms of host metabolic and immune modulation. We also examine cross-compartment interactions, emerging multi-omics approaches, and the translational potential of microbiota-targeted interventions. Oral pathogens promote systemic inflammation and endothelial activation. Gut-derived metabolites such as TMAO exacerbate foam cell formation and impair reverse cholesterol transport, whereas SCFAs exert protective effects via immune modulation and gut barrier maintenance. Emerging evidence suggests that blood microbial components contribute to vascular inflammation, though methodological challenges remain. Multi-omics integration (metagenomics, metabolomics, host genomics) reveals interconnected metabolic networks linking microbial activity to atherosclerosis. Microbiota-targeted strategies, including dietary modulation, TMA lyase inhibitors, and probiotics, show promise for risk stratification and therapeutic intervention. The human microbiota regulates atherosclerosis through immunometabolic metabolites, offering promising biomarkers and therapeutic targets. However, clinical translation requires addressing interindividual variability, establishing causality, and standardizing methodologies. This review provides an integrated framework for leveraging microbiota-host interactions in precision cardiovascular medicine.

Interbacterial adhesion is central to multispecies biofilm formation. Streptococcal serine-rich repeat glycoproteins (SRRPs) play a well-defined role in oral colonization, yet SRRP involvement in interbacterial adhesion remains understudied. Here, we aimed to isolate SRRP-dependent adhesion partners of Streptococcus gordonii Challis (DL1) from human oral microbiota. Of 179 isolates screened, 23 coaggregated with DL1 but not with an isogenic SRRP-encoding gene deletion mutant. Whole-genome sequencing identified isolates as 19 Schaalia odontolytica, 3 Schaalia sp. HMT-172, and 1 non-Schaalia mixed-species isolate. Each Schaalia isolate also coaggregated with other oral streptococcal species that encoded SRRPs. When Sch. spp. whole cells were probed with a recombinant DL1 SRRP binding domain, which binds to sialic acids, no binding was observed. Formaldehyde and heat treatment of Sch. spp. cells to denature surface proteins reduced coaggregation with DL1 cells, whereas the same treatment of DL1 did not affect coaggregation with Sch. spp. Proteinase K treatment of DL1 or Sch. spp. reduced or eliminated coaggregation, respectively. Based on these observations, we propose that Sch. odontolytica and Sch. sp. HMT-172 surface proteins bind to formaldehyde- and heat-stable epitopes of streptococcal SRRPs, potentially constituting an important interbacterial adhesion interaction in oral biofilm formation.

Nicotine Vapes have experienced a rise in their popularity, and our understanding of how vapes affect our oral microbiome remains to be reviewed. This systematic review explores whether the use of vapes is associated with measurable alterations in the diversity and taxonomic composition of the oral microbiome compared to non-vapers or conventional cigarette smokers. A comprehensive and systematic search of 6 databases was meticulously conducted, covering published literature up to the end of August 2024. The data was then extracted and underwent a qualitative analysis. Studies' risk of bias was assess using Newcastle Ottawa Scale Eligible studies needed to have a comparison group of either non-smokers or tobacco users or both and a group of sole e-cigarette users. The search yielded 18 articles, with sixteen being cross-sectional and the remaining two were cohort studies. There were 1418 participants across the studies, ranging from 30-125 participants in each study. Majority of the included literature indicated e-cigarettes can alter the taxonomic composition and diversity of their user's oral microbiome. Vaping was found to be associated with changes in oral microbiome. Since, the majority of the existing literature relied on self-reporting to see if participants were sole vapers, and mainly focused on bacterial genera, the exact impact of these changes are difficult to ascertain. However, the existing literature demonstrates a relationship in a few bacterial genera associated with periodontal disease among e-cigarette users, highlighting the need for further comprehensive studies with sound methodological approach to recruit sole e-cigarette users. This study concludes that nicotine vapes do have a demonstratable impact on the oral microbiome that is unique to vapes. E-cigarette use may be associated with an increase periodontal pathogens which may predispose e-cigarette users to worse periodontal disease, however, further research is required.

Infection with the bacterium C. perfringens in sheep and goat herds leads to considerable losses. The most common diseases in small ruminants caused by this bacterium are pulpy kidney disease, enterotoxaemia, yellow lamb disease, and necrotic enteritis. C. perfringens is widely distributed in the environment and is part of the intestinal microbiota of humans and animals. When physiological conditions in the body change, it begins to produce toxins that lead to various pathological changes. Depending on the toxins it produces, it is classified into seven types (A–G), defined based on the presence of genes encoding the CPA toxin (all types), CPB toxin (type B and type C), ETX toxin (type B and D), ITX toxin (type E), CPE toxin (type F) and NetB toxin (type G). Strains A and D are most commonly associated with enterotoxaemia in small ruminants. According to the available literature, C. perfringens toxinotype A is most frequently isolated in small ruminant herds. In addition to toxin genes, antibiotic resistance genes also play an important role in bacterial survival. Of the genetic determinants of antimicrobial resistance discovered to date, most are associated with the following antimicrobial drugs: bacitracin (bcrR gene), tetracyclines (tet genes), macrolides (erm genes), lincosamides (erm and lnu genes), streptogramins (erm genes) and chloramphenicol (cat genes). Due to sudden death after the onset of symptoms and the economic unprofitability, very few results are available on antibiotic resistance of C. perfringens in small ruminants. Therefore, it has proven to be more economical and effective to work on prevention than on treatment. Since there is no vaccine against enterotoxaemia in Croatia, prevention of the disease is difficult.

The Human Microbiome in Airborne Particulate Matter–Associated Aging-Related Chronic Diseases: An Evidence-Stratified Review

Cerebellar Abscess Caused by Rare Bacteria: A Case Report.

The healthy gut microbiota communities play a complex and significant role in lipid absorption and deposition, leading to multiple health benefits. Here, we confirmed an impaired absorption and deposition function in germ-free pigs and mice, which was partially reversed after human fecal microbiota transplantation. By integrating single-cell data from adipose tissue, we identified HDAC9 as a key regulator, marked by the presence of a population of small mature adipocytes exhibiting high HDAC9 and low PPARγ expression in germ-free pigs. HDAC9 deficiency of preadipocytes drove FABP4/5-mediated lipid deposition by directly targeting PPARγ expression and acetylation modification. Finally, we verified the interaction between gut microbiota and host HDAC9/PPARγ/FABP4/5 signaling cascade might be microbial receptors (ie, Dectin1 or TLRs)-dependent rather than microbial metabolites. Altogether, our study uncovers the gut microbiota-HDAC9-PPARγ axis as a key regulator of adipocyte function and lipid deposition, offering a potential therapeutic target for lipid-related metabolic diseases.

MICROBIOME: A DRIVER OF PANCREATIC INFLAMMATION AND TUMORIGENESIS

Dietary tryptophan enhances aryl hydrocarbon receptor activation and reduces colitis through microbial metabolism.

Colorectal cancer (CRC) progression is closely associated with gut microbiota. Bacteroides thetaiotaomicron (B.theta), a key species in the human cecal and colonic microbiota, plays an incompletely defined role in CRC progression. CRC animal models were established utilizing immunocompetent C57BL/6 mice and immunodeficient BALB/C nude mice. Histopathological changes were assessed by H&E staining. Immune cell infiltration was evaluated by IHC. CD8+ T cells and cancer cells were treated with B.theta culture supernatant. Cytokine secretion was measured by ELISA. Surface protein expression levels on CD8+ T cells and cancer cell apoptosis were analyzed by flow cytometry. CD8+ T cell proliferation was determined by the CFSE assay. Tumor-killing activity of CD8+ T cells was assessed by LDH release assay. In C57BL/6 mice, B.theta suppressed tumor development and promoted T cell infiltration. However, B.theta had no significant impact on CRC progression in BALB/C nude mice. B.theta supernatant treatment did not affect CRC cell phenotypes, including viability, apoptosis, MHC-I expression, and extracellular ATP levels. Conversely, B.theta supernatant upregulated CD69 and CD44 expression on CD8+ T cells, promoted IFN-γ and TNF-α secretion, enhanced proliferation, and consequently augmented their cytotoxicity against CRC cells. B.theta suppresses malignant CRC progression by modulating host immune responses.