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PubMed2026

Identification of a novel human gut microbes and microbial metabolites related genes signature for prognostic implication in head and neck squamous carcinomas.

BACKGROUND: The gut microbiota acts as a critical driver influencing the pathogenesis, therapeutic response, and clinical outcomes across various cancer types. This study aimed to investigate the prognostic value of human gut microbes and microbial metabolites related genes (HGMMMRGs) in head and neck squamous cell carcinoma (HNSCC). METHODS: We constructed a prognostic risk model comprising 19 core HGMMMRGs using LASSO penalized regression and a multivariate Cox proportional hazards model. The predictive performance of the model was evaluated through Kaplan-Meier analysis, receiver operating characteristic (ROC) curves, nomograms, and concordance index. In addition, functional enrichment analysis was performed on the differentially expressed risk genes. Furthermore, the relationship between the immune microenvironment of HNSCC and the risk diagnostic model was examined. Western blot analysis was used to assess the expression levels of IL10 in both HNSCC tissues and adjacent normal tissues. Finally, the correlation between IL10 and the gut microbiota was explored. RESULTS: This study developed a risk score model integrating 19 HGMMMRG genes, which can serve as a tool to guide prognosis and immune microenvironment assessment in HNSCC patients. Survival analysis showed that patients in the high-risk group had significantly worse outcomes (P < 0.05). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis revealed significant enrichment of differentially expressed genes (DRLs) and immune-related pathways. Western blot analysis further confirmed that IL10 was highly expressed in HNSCC, and the abundance of Faecalibacterium prausnitzii and Enterococcus durans colonies was correlated with IL10 expression. CONCLUSION: We developed a prognostic model for HGMMMRGs that can be effectively used to predict OS in patients with HNSCC. Second, Faecalibacterium prausnitzii and Enterococcus durans can influence the prognosis of patients with HNSCC by mediating the expression IL10 and thereby affecting the prognosis of HNSCC patients. Thus, human gut microbes and microbial metabolite-related genes may be another promising strategy for the treatment of patients with HNSCC.

HNSCC↗

PubMed2024

Obesity-enriched gut microbe degrades myo-inositol and promotes lipid absorption.

Numerous studies have reported critical roles for the gut microbiota in obesity. However, the specific microbes that causally contribute to obesity and the underlying mechanisms remain undetermined. Here, we conducted shotgun metagenomic sequencing in a Chinese cohort of 631 obese subjects and 374 normal-weight controls and identified a Megamonas-dominated, enterotype-like cluster enriched in obese subjects. Among this cohort, the presence of Megamonas and polygenic risk exhibited an additive impact on obesity. Megamonas rupellensis possessed genes for myo-inositol degradation, as demonstrated in vitro and in vivo, and the addition of myo-inositol effectively inhibited fatty acid absorption in intestinal organoids. Furthermore, mice colonized with M. rupellensis or E. coli heterologously expressing the myo-inositol-degrading iolG gene exhibited enhanced intestinal lipid absorption, thereby leading to obesity. Altogether, our findings uncover roles for M. rupellensis as a myo-inositol degrader that enhances lipid absorption and obesity, suggesting potential strategies for future obesity management.

Inositol↗

PubMed2026

Substrate recognition and cleavage by mucin degrading O-glycopeptidases from the gut microbe Bacteroides caccae.

O-glycopeptidases are enzymes that hydrolyze the peptide bonds in glycoproteins by a mechanism that involves specific recognition of O-linked glycans on the substrate. Bacteroides caccae, an accomplished mucin degrader, is a member of the human gut microbiota with sixteen genes encoding putative O-glycopeptidases in the peptidase_M60 family. At present, the diversity of substrate selectivity in O-glycopeptidases is not well-understood, nor is the rationale behind their expansion in bacteria such as B. caccae. Here, we reveal the activity and diversity of the peptidase_M60 O-glycopeptidases encoded in the B. caccae genome. At least thirteen of the sixteen peptidase_M60 encoding genes produce active mucinolytic enzymes. Targeted functional studies by a high-throughput FRET screen combined with detailed kinetic analyses reveal that five examples in an uncharacterized clade of peptidase_M60 proteins are specifically O-glycopeptidases with different substrate selectivities despite their relatively high degree of relatedness. Structural analyses of these enzymes, including bound complexes, reveal new insight into the molecular underpinnings of O-glycopeptidase diversity. This highlights the larger context of how varied the selectivity of peptidase_M60 O-glycopeptidases can be for the glycan moiety and/or the peptide portion of the substrates, and why mucin degraders like B. caccae diversify O-glycopeptidase substrate repertoires to potentially maximize breakdown of this extraordinarily complex polymer.

Mucins↗

PubMed2024

Metagenomic Analysis of Gut Microbiome of Persistent Pulmonary Hypertension of the Newborn.

Persistent pulmonary hypertension of the newborn (PPHN) is one of the most common diseases in the neonatal intensive care unit which severely affects neonatal survival. Gut microbes play an increasingly important role in human health, but there are rarely reported how gut microbiota contribute to PPHN. In our study, the metagenomic sequencing of feces from 12 PPHN's neonates and 8 controls were performed to expose the relation between neonatal gut microbes and PPHN disease. Firstly, we found that the abundance of Actinobacteria, Proteobacteria, Bacteroidetes were significantly increased in PPHN compared with controls, but the Firmicutes components was reduced. And some pathogenic strains (like Vibrio metschnikovii) were significantly enriched in the PPHN compared with controls. Secondly, functional annotation of genes found that PPHN up-regulated transmembrane transport, but down-regulated ribosome and ATP binding. Lastly, microbial metabolic pathway enrichment analysis indicated that some metabolic pathway in PPHN were conflicting and contradictory, showed that an abnormally increased metabolism, disturbed protein synthesis and genomic instability in the PPHN neonate. Our results contribute to understanding the changes in the species and function of gut microbiota in PPHN, thus providing a theoretical basis for the explanation and treatment of PPHN.

Gastrointestinal Microbiome↗

PubMed2026

Immunological, Inflammatory, and Microbiota Determinants of Carpal Tunnel Syndrome: Evidence from Mendelian Randomization.

INTRODUCTION: Carpal Tunnel Syndrome (CTS) is a common peripheral neuropathy, and immune dysregulation and microbial dysbiosis are believed to play a role in its development. However, the cause-and-effect relationships have yet to be clarified. METHODS: Using publicly available Genome-Wide Association Study (GWAS), there are 731 immune cell phenotypes, 91 inflammatory proteins, 150 skin microbiota taxon, and 473 gut microbiota taxon based on two-sample Mendelian Randomization (MR) analysis to test whether there is a causal relationship between them and CTS. The results from the study were shown to have some degree of stability as demonstrated by various sensitivity analyses, which included running heterogeneity tests, performing MR -PRESSO, and running MR-Egger regressions. On the other hand, reverse MR was performed to verify the direction of the association. In addition, a two-step MR mediation analysis was conducted to explore whether there was a mediation effect of gut microbiota and skin microbiota, respectively, of immune and inflammatory traits on CTS. RESULTS: 22 Immune cell traits, 4 Inflammatory proteins, 18 gut microbiota taxa, and 3 skin microbiota taxa are causally associated with CTS. Reverse MR suggested feedback effects of CTS on select immune traits and gut microbiota. Mediation analysis revealed 4 gut microbiota taxa that substantially mediated immune/inflammatory effects upon CTS, with mediation rates as high as 44%; however, skin microbiota did not demonstrate any mediation. DISCUSSION: The immune dysregulation, inflammation, and the gut microbiota that cause CTS are all revealed through this research. Mendelian randomization analysis suggests that traits and inflammatory proteins of immune cells directly increase the risk of CTS, and certain types of gut microbes partially mediate these effects. Therefore, the results show a central role of the immune-gut axis in CTS pathogenesis, and suggest a systemic, rather than a local, immune-microbial interaction in disease development. CONCLUSION: We provided the first causal evidence that immune cells, inflammatory proteins, and CTS risk are causally associated with some specific taxa of gut microbiota. This contributes to a better understanding of the immune-microbiome interactions in the process of occurrence and development of CTS, and also provides theoretical support for precision prevention and treatment.

Humans↗

PubMed2026

Genome-resolved analysis reveals disruption of gut microbial vitamin B and K2 biosynthesis during Toxoplasma gondii infection in mice.

UNLABELLED: Toxoplasma gondii infection remodels the gut microbiome, yet its impact on microbial vitamin biosynthetic potential and host redox metabolism remains unclear. Here, we integrated mouse gut metagenomes with publicly available metagenome-assembled genomes (MAGs) to construct a genome-resolved atlas of B-vitamin and vitamin K2 biosynthesis. From 45,697 MAGs, we curated 4,771 representative genomes, of which 2,682 met high-quality criteria (completeness ≥90%, contamination <5%). Functional annotation identified 229,717 vitamin-related genes corresponding to 177 Kyoto Encyclopedia of Genes and Genomes (KEGG) orthologs across de novo pathways for eight B vitamins, thiamine (B1), riboflavin (B2), niacin (B3), pantothenate (B5), pyridoxine (B6), biotin (B7), folate (B9), cobalamin (B12), and vitamin K2. Among the high-quality genomes, 1,665 encoded complete de novo pathways for at least one vitamin, highlighting functional specialization and community-level complementarity. Transcripts per million-normalized metagenomic read counts revealed significant differences in KEGG ortholog abundances across six of the nine vitamin pathways. Reanalysis of metagenomic data from infected mice (acute, chronic, and control; n = 10 per group) revealed a stage-dependent reduction in α-diversity of vitamin biosynthesis pathways during acute infection, and a clear β-diversity separation from chronic and control groups. Core niacin biosynthesis genes (nadB, nadA, nadC) displayed phylum-specific redistribution, indicating selective remodeling of microbial NAD+ precursor production under infection-induced metabolic stress. These results suggest that T. gondii infection disrupts cooperative vitamin biosynthetic networks while specifically modulating niacin pathways linked to host NAD+ metabolism. IMPORTANCE: Gut microbes can synthesize essential vitamins, but how infection alters this function is poorly understood. By integrating mouse gut metagenomes with genome-resolved microbial data, we show that Toxoplasma gondii infection reshapes the vitamin biosynthetic potential of the gut microbiome in a stage-dependent manner. Acute infection reduces the diversity of vitamin biosynthesis pathways and shifts the taxonomic distribution of key niacin biosynthesis genes involved in microbial NAD+ precursor production. These findings identify vitamin metabolism, especially niacin-related pathways, as a sensitive functional axis of microbiome remodeling during infection. Our work links microbial taxonomic changes to functional metabolic consequences and suggests that microbiome-mediated regulation of NAD+-related metabolism may contribute to host redox adaptation during T. gondii infection.

B vitamins↗

PubMed2026

Microbiota-gut-muscle axis shapes fish muscle texture by regulating collagen synthesis.

BACKGROUND: Increasing studies have emphasized the communication network between the gut microbiome and host organs, revealing that such interactions significantly influence host physiological performances. However, whether a gut-muscle axis exists to regulate muscle quality in animal production is unknown. RESULTS: In two independent cohorts, the muscle hardness of tilapia subjected to a long-term faba bean diet exhibited significant inter-individual variation. RNA-Seq analyses of the high-hardness (H) and low-hardness (L) groups pointed to collagen-based extracellular matrix as a possible factor driving muscle hardness development. Transplantation of gut microbiota from the H donor resulted in enhanced collagen synthesis in gnotobiotic zebrafish. Muscular collagen deposition was featured with an increased abundance of gut Cetobacterium. Gnotobiotic models colonized with live C. somerae exhibited enhanced collagen synthesis. Integrated analyses of microbiome function, bacterial genome, and metabolic profiles identified acetate as a key effector of C. somerae. Acetate incubation upregulated collagen I expression in TGF-β-activated fibroblasts in an acetylation-dependent manner. Mechanistically, acetate promoted the acetylation of SMAD2/3, enhancing its nuclear transport and stability, which ultimately increased collagen expression. An acetate-supplemented feeding experiment corroborated these findings. CONCLUSION: The comprehensive results provided evidences that gut microbes regulated tilapia muscle texture through SMAD2/3 acetylation-driven collagen synthesis. This study expands our understanding of the multifaceted role of the gut-muscle axis in muscle physiology. Furthermore, our findings highlight that targeting gut microbiota and the downstream collagen synthesis pathway could be promising for manipulating muscle quality in animal production. Video Abstract.

Animals↗

PubMed2026

Gut Microbiome Composition Is Associated With Response to CD38 Antibody (Daratumumab) Treatment Among Relapsed Multiple Myeloma Patients.

INTRODUCTION: Growing data support interactions between host-gut microbes and treatment responses in multiple myeloma (MM), where a higher abundance of Eubacterium hallii in stool samples has been found among MM patients with negative minimal residual disease after induction therapy. Here, we evaluated changes in the gut microbiome associated with daratumumab (dara) based therapy in 40 MM patients, before and after therapy. PATIENTS AND METHODS: Patients with relapsed MM and prior autologous transplantation who had received 1 to 4 prior lines of therapy were eligible. Two stool samples were collected, one within 1 week prior to dara (predara) and one immediately after 4 doses of dara (postdara). Metagenomics sequencing was conducted. Microbiome taxonomic analyses were performed using MetaPhlAn4, and microbial functional pathway analyses were conducted using HUMAnN3.6. QIIME2 was used for compositional and statistical analyses. RESULTS: Of 40 participants enrolled, there were 5 nonresponders; 35 patients achieved partial response (PR) or better (responders). Among responders, 10 patients achieved complete remission (CR), and 25 patients achieved either very good partial response (VGPR) or PR. There were no statistically significant differences between overall pre and postdara gut microbiomes. Differential abundance analysis (ANCOM-BC) showed statistically significant (q ≤ 0.05) overgrowth of Alistipes finegoldii and Acidaminococcus intestini species in responders and Ruminococcus torques, Sellimonas intestinalis and Clostridium symbiosum in nonresponders. Compared to non-CR, CR samples showed enrichment of Faecalibacterium prausnitzii; non-CR samples were enriched in Segatella copri and Faecalimonas umbilicata. DISCUSSION/CONCLUSION: Our results suggest differences in species between clinical responders and nonresponders, but larger prospective studies are needed to confirm these results.

Clinical response↗

PubMed2025

Human xenobiotic metabolism proteins have full-length and split homologs in the gut microbiome.

Xenobiotics, including pharmaceutical drugs, can be metabolized by both host and microbiota, in some cases by homologous enzymes. We conducted a systematic search for all known human proteins with gut microbial homologs. Because gene fusion and fission can obscure homology detection, we built a pipeline to identify not only full-length homologs, but also cases where microbial homologs were split across multiple adjacent genes in the same neighborhood or operon ("split homologs"). We found that human proteins with full-length gut microbial homologs disproportionately participate in xenobiotic metabolism. While this included many different enzyme classes, short-chain and aldo-keto reductases were the most frequently detected, especially in prevalent gut microbes, while cytochrome P450 homologs were largely restricted to lower-prevalence facultative anaerobes. In contrast, human proteins with split homologs tended to play roles in central metabolism, especially of nucleobase-containing compounds. We identify twelve specific drugs that gut microbial split homologs may metabolize; 2 of these, 6-mercaptopurine by xanthine dehydrogenase and 5-fluorouracil by dihydropyrimidine dehydrogenase, have been recently confirmed in mouse models. This work provides a comprehensive map of homology between the human and gut microbial proteomes, indicates which human xenobiotic enzyme classes are most likely to be shared by gut microorganisms, and finally demonstrates that split homology may be an underappreciated explanation for microbial contributions to drug metabolism.

Humans↗

PubMed2026

Bacteria and phage consortia modulate cecal SCFA production and host metabolism to enhance feed efficiency in ducks.

BACKGROUND: The gut microbiota influences poultry health, nutrition, feed efficiency (FE), and overall productivity. However, the relationship between gut microbes, including bacteria and phages, and FE in ducks remains underexplored. To address this, we integrated cecal 16S amplicon, metagenome, microbiota-derived short-chain fatty acids (SCFAs) profiling, liver transcriptome, and serum metabolome data to illustrate the contribution of the gut microbiome (bacteria and viruses) to duck FE. RESULTS: We reconstructed viral genomes and prokaryotic metagenome-assembled genomes (MAGs) and annotated their genes using comprehensive databases. Prokaryotic hosts of viruses were also predicted to understand virus-host dynamics within the gut ecosystem. Our results revealed that high-FE ducks have higher concentration of propionate and butyrate in cecum compared with low-FE ducks. The metagenome sequencing revealed distinct cecal microbiota profiles between two groups, with increased relative abundance of representative SCFA producers, especially Paraprevotella sp905215575 and Bacteroides sp944322345, and enhanced SCFA-biosynthesis pathways in high-FE ducks. Virome genome assembly identified two phages encoding auxiliary metabolic genes (AMGs) involved in pyruvate metabolism, enhancing nutrient availability for host bacteria to produce SCFAs (e.g., temperate phage-encoded pyruvate phosphate dikinase) or exploiting host central metabolic pathways for viral replication (e.g., lytic phage-encoded formate C-acetyltransferase). Furthermore, these representative SCFA-producing bacteria and phage consortia were associated with serum metabolites (including L-histidine and 4-hydroxydecanedioylcarnitine) linked to duck FE. CONCLUSION: Collectively, these findings provide novel insights into the gut microbial factors regulating FE in ducks, offering potential strategies to optimize poultry nutrition and productivity. Video Abstract.

Animals↗

PubMed2025

Human gut Bifidobacterium longum subsp. suillum is enriched in vitro by a pectic polysaccharide isolated from the flowers of Lilium lancifolium.

Although pectins have been explored widely, knowledge of their effects on the gut microbiota is lacking owing their complex structure. The aim of this study was to investigate whether pectin enriched gut microbes in vitro. To address this, a homogeneous RG-I like pectin, L01-B1, with a molecular weight of 43.9 kDa was extracted from the flowers of Lilium lancifolium. Structural analysis revealed that L01-B1 contained rhamnose, glucuronic acid, galacturonic acid, galactose, and arabinose in a molar ratio of 13.4: 1.8: 11.1: 37.2: 36.5. The backbone of L01-B1 was composed of 1, 6-β-Galp, 1, 4-α-GalpA, and 1, 2-α-Rhap, whereas the branches included 1, 5-α-Araf, 1, 4-β-Galp, and T-β-GlcpA attached to C-4 of rhamnose, and 1, 3-β-Galp and T-β-Galp linked to C-3 of galactose. L01-B1 altered the composition of human gut microbiota in vitro and increased the abundance of Bifidobacterium longum. Furthermore, Bifidobacterium longum subsp. suillum strain DK001 was isolated and identified from human feces. The DK001 genome was found to be circular with a genome size of approximately 2.4 M. Notably, L01-B1 might possibly be degraded by two kinds of enzymes and change the metabolism of human gut microbiota. Overall, these findings provide insights into intervention strategies that target Bifidobacterium longum.

Humans↗

PubMed2025

Systematic identification and characterization of regulators of aryl hydrocarbon receptor signaling.

The human aryl hydrocarbon receptor (AHR) integrates chemical signals derived from the environment, gut microbes, and endogenous sources to regulate processes ranging from intestinal barrier integrity to xenobiotic detoxification. Despite strong evidence that dysregulation of AHR signaling is a causal factor in metabolic and autoimmune disorders, we currently lack a comprehensive understanding of the factors that regulate AHR activity in human cells. Here, we use genome-scale CRISPR screening to systematically identify regulators of AHR signaling in hepatocytes. The resulting datasets recapitulate the core AHR signaling pathway and identify a large network of regulators. Many of these factors have roles beyond AHR signaling, reflecting that AHR signaling is deeply integrated into human cell biology. We further dissect this network to reveal novel modes of regulation of AHR expression, protein levels, and signaling. For example, we find that the E3 ubiquitin ligase UBR5 sustains AHR signaling by counteracting degradation of ligand-bound AHR. Finally, we identify components of the AHR regulatory network that are specific to cell types and ligands as potential nodes to manipulate AHR signaling in a targeted manner for therapeutic benefit. Overall, our results define the regulatory network that underpins AHR activation, with implications for our understanding of host-microbe interactions and integrative chemosensation and the etiology of metabolic and inflammatory disorders.

Journal Article↗

PubMed2026

Proteobacteria with chemosynthetic potential are highly prevalent in the gills of Hypoplectrus reef fishes.

Fishes host a diverse microbiome in their gills, but a broad characterization of this microbiome at the metagenomic level is lacking. Here, we apply genome-resolved metagenomics to the gills of the hamlets (Hypoplectrus spp), a group of reef fishes from the Greater Caribbean. The analysis of 353 gill samples from 15 hamlet species collected at eight locations over 13 years revealed a stark contrast between the gill microbiota and reef water microbial communities, indicating a distinct and specific gill microbiome. A total of 70 gill-associated metagenome-assembled genomes (MAGs) were recovered. These MAGs belong to 17 lineages, most of which are novel. They relate to known fish gill pathogens, fish gut microbes, free-living and biofilm-associated taxa, indicating that the gill microbiome was assembled from a collection of distinct eco-evolutionary trajectories. The MAGs harbor diverse metabolic modules, involved notably in nitrogen cycling, antibiotic production and biofilm formation, revealing a highly dynamic microbial ecosystem. One lineage in the Burkholderiaceae family was outstandingly prevalent across fish host species, sampling locations and years. Its genome encoded complete metabolic modules for carbon fixation and sulfur oxidation, indicating chemosynthetic potential. To the best of our knowledge, this is the first line of evidence that fishes may host sulfur-oxidizing chemosynthetic bacteria in their gills. The functional significance of this chemosynthetic potential for the fish host or other members of the gill microbiome remains to be established. The high prevalence of this lineage allowed to build a pangenome. It revealed large-scale geographic structure (western Caribbean, eastern Caribbean and Gulf of Mexico), which parallels the phylogenomic pattern observed in the hamlets. Overall, our findings point to complex fish host-microbe and microbe-microbe eco-evolutionary interactions in the gills that may influence fish physiology, homeostasis and immune response.

Animals↗

PubMed2025

Gut metagenome and plasma metabolome profiles in older adults suggest pyruvate metabolism as a link between sleep quality and frailty.

Poor sleep quality is associated with increased frailty in older adults, but the role of the gut microbiome in this relationship remains unclear. Here, gut metagenome and plasma metabolome were profiled in 1,225 individuals aged 62-96 years. Poor sleep quality was associated with reduced abundances of potential probiotics such as Faecalibacterium prausnitzii and elevated abundances of pathobionts. A gut microbiome sleep quality index (GMSI) was developed to quantify microbial balance related to better sleep quality; higher GMSI scores were inversely associated with frailty and related clinical traits. Pyruvate metabolism emerged as a key microbial pathway linking sleep quality to frailty, with features such as F. prausnitzii abundance and microbial pyridoxal 5'-phosphate biosynthesis implicated in this connection. These findings deepen our understanding of microbiome-metabolome pathways related to sleep quality and frailty in aging and provide a valuable resource for future longitudinal and interventional studies.

Humans↗

PubMed2025

Gut fungi are associated with human genetic variation and disease risk.

Human genetic determinants of the gut mycobiome remain uninvestigated despite decades of research highlighting tripartite relationships between gut bacteria, genetic background, and disease. Here, we present the first genome-wide association study on the number and types of human genetic loci influencing gut fungi relative abundance. We detect 148 fungi-associated variants (FAVs) across 7 chromosomes that statistically associate with 9 fungal taxa. Of these FAVs, several occur in the protein-coding genes PTPRC, ANAPC10, NAV2, and CDH13. Additional FAVs link to tissue-specific gene expression as fungi-associated expression quantitative trait loci. Notably, the relative abundance of gut yeast Kazachstania associates with genetic variation in CDH13 encoding T-cadherin, a protein linked to cardiovascular disease. Kazachstania forms a causal relationship with cardiovascular disease risk in a mendelian two-sample randomization analysis. These findings establish previously unrecognized connections between human genetics, gut fungi, and chronic disease, broadening the paradigm of human-microbe interactions in the gut to the mycobiome.

Humans↗

PubMed2026

Harnessing Probiotic LAB and Bacteriocins for Clean-Label Food Processing and Biopreservation: Omics, Molecular Innovations and Industrial Applications.

The persistence of microbial agents in foods, especially spore forming bacteria is one of the most significant challenges to food preservation and safety, undermining product quality, shelf life, and consumer health. The use of traditional control methods, including thermal processing and chemical preservatives, are increasingly limited by consumer demands for minimally processed foods, and the emergence of resistant microbial strains. Advances have been made in the use of probiotics like lactic acid bacteria (LAB) and their biometabolites like bacteriocins in food processing and preservation, particularly to control biofilm and endospore forming pathogens including Bacillus sp., Listeria sp., Staphylococcus sp., Clostridium sp., E. coli etc. in foods and food processing plants/surfaces. Given the ability of these organisms to cause foodborne illness and form resilient biofilms in the food processing ecosystem and their resistance to the conventional method of their elimination, the antimicrobial peptides (bacteriocins) are gaining increasing prominence as useful alternatives to synthetic antimicrobials in enhancing food safety and combating the threats of these pathogens. This review addresses current information on the inhibition of persistent microbial spoilage contaminants, biofilm-forming pathogens, and spore formers of interest to the food industry using LAB and their bacteriocins. Current developments in isolation, characterization, and mode of action of bacteriocins are explored, including synergistic activity with other preservative hurdle techniques such as encapsulation, and nanobiotechnology. Importantly, there is a focus on the utilization of molecular and omics-based approaches to enable a better understanding of bacteriocin biosynthesis, gene regulation, host-microbe interactions and gut microbiome regulation potential of probiotic LABs, permitting the rational development of targeted and strain-specific interventions. Developments in the incorporation of bacteriocin-producing LAB into functional starter cultures and bio-protective products, and challenges in stability, regulatory approval, and scalability for industrial use, are also discussed in the paper. Despite their considerable potential, broader translation remains constrained by regulatory requirements, production and formulation costs, variable efficacy in complex food matrices, and the limited validation of many candidate bacteriocins beyond laboratory and model-food systems. Collectively, these advances position LAB and their bacteriocins at the leading edge of developing sustainable, clean-label, and efficacious functional foods and food preservation systems. Their functionality can be expanded by integrating genomics, synthetic biology, and predictive modeling for the maximization of their biopreservative potential in diverse food matrices and in gut microbiota modulation.

Bioactive Peptides↗

PubMed2024

Revealing novel protein interaction partners of glyphosate in Escherichia coli.

Despite all debates about its safe use, glyphosate remains the most widely applied active ingredient in herbicide products, with renewed approval in the European Union until 2033. Non-target organisms are commonly exposed to glyphosate as a matter of its mode of application, with its broader environmental and biological impacts remaining under investigation. Glyphosate displays structural similarity to phosphoenolpyruvate (PEP), thereby competitively inhibiting the 5-enolpyruvylshikimate-3-phosphate synthase (EPSPS), crucial for the synthesis of aromatic amino acids in plants, fungi, bacteria, and archaea. Most microbes, including the gut bacterium Escherichia coli (E. coli), possess a glyphosate-sensitive class I EPSPS, making them vulnerable to glyphosate's effects. Yet, little is known about glyphosate's interactions with other bacterial proteins or its broader modes of action at the proteome level. Here, we employed a quantitative proteomics and thermal proteome profiling (TPP) approach to identify novel protein binding partners of glyphosate in the E. coli proteome. Glyphosate exposure significantly altered amino acid synthesizing pathways. The abundance of shikimate pathway proteins was increased, suggesting a compensatory mechanism. Extracellular riboflavin concentrations were elevated upon glyphosate exposure, while intracellular levels remained stable. Beyond the target enzyme EPSPS, thermal proteome profiling indicated an effect of glyphosate on the thermal stability of certain proteins, including AroH and ProA, indicating interactions. Similar to the competitive binding between PEP and glyphosate at EPSPS, one reason for the interaction of AroH and ProA with the herbicide could be a high structural similarity between their substrates and glyphosate. Overall, glyphosate induced metabolic disturbances in E. coli, extending beyond its primary target, thereby providing new insights into glyphosate's broader impact on microbial systems.

Glyphosate↗

PubMed1979

[Structural characteristics of the mucosa of the small intestine in gnotobiote rats].

Histological and electron microscopic investigations of mucosal strucutre of the small intestine in gnotobiotic and conventional rats have demonstrated that mucosal index (lenear dimentions of villi/crypt dimentions ratio) is equal to 3--4 and 1.4--2.5, respectively. In gnotobiotic rats the number of mitotic figures in crypts is less, migratory-desquamative parameters of enterocytes are 5--6 days, cranio-caudal gradient of linear dimentions of villi, crypts and the number of goblet-shaped cells is not expressed. The goblet-shaped cells and cells with acidophilic granules have secretion of moderate intensity. The number of cells infiltrating epithelium of villi and crypts is greater when microbes are present in the gut lumen. A considerable difference in the structure of the connective tissue basis of the gnotobiotic and conventional rats mucosa are also connected with presence or absence of microflora in the gut lumen.

Animals↗