PubMed HealthSearch

Biomedical subjects

Jing Jiang

Publications and source records attributed to Jing Jiang.

3 recordsLinked to original sources

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 &#x2265;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 &#x3b1;-diversity of vitamin biosynthesis pathways during acute infection, and a clear &#x3b2;-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

Genome-resolved analysis of colonization factor repertoires reveals ecological stratification in cervid gut microbiomes.

INTRODUCTION: Colonization factors (CFs) are important microbial traits associated with persistence and host adaptation in the gut, yet their large-scale organization in cervid gut microbiomes remains unclear. METHODS: A total of 3,311 non-redundant high-quality metagenome-assembled genomes (MAGs), derived from 688 cervid gut metagenomic samples across 15 publicly available projects and one in-house dataset, were analyzed. CF-associated genes were identified by comparison against the GHA CF database, and CF repertoires were characterized at genome, host-species, and gastrointestinal-segment levels. RESULTS: A total of 138,729 CF-associated genes spanning 71 CF families were identified. MAGs from Cervinae contained richer CF repertoires than those from Caprinae, and CF47 (Peptidase_C69), CF24_29 (QueH), and CF18 (Glycos_transf_2) were among the most prevalent families. CF repertoires were strongly structured by taxonomy, showed a moderate association with bacterial phylogenetic distance, and formed two recurrent genome-level configurations with distinct KEGG functional profiles. Integration of sample metadata further revealed differentiation of CF repertoires across host species and gastrointestinal segments, representing the major ecological dimensions examined in this study. Segment-associated CF variation was accompanied by redistribution of broader functional profiles, including enrichment of carbohydrate and lipid metabolism in the jejunum, membrane transport in the ileum, xenobiotics biodegradation in the cecum, and environmental adaptation in the rumen. DISCUSSION: These findings provide a genome-resolved view of CF repertoire organization in cervid gut microbiomes and demonstrate that colonization-associated functions are structured across microbial lineages and ecological contexts. This study highlights the importance of considering microbial taxonomy and host-associated environments when interpreting the distribution of CF repertoires in mammalian gut ecosystems.

Cervidae

CD4+CD8+ double-positive T cells are associated with severity of tuberculosis.

BACKGROUND: Tuberculosis (TB) remains a global public health burden, and how immune cell subsets regulate host anti-TB immunity and disease progression remains incompletely understood. While previous studies have focused on single-positive (SP) T cells (CD4+ or CD8+) in TB pathogenesis, the association between CD4+CD8+ double-positive (DP) T cells and TB susceptibility, severity, and treatment outcomes have not been fully elucidated. This study aimed to investigate the relationship between DP T cells and other immune cell subsets with TB, and to explore the potential diagnostic and prognostic value of DP T cells in active TB. METHODS: A Genome-Wide Association Study (GWAS) was conducted to analyze 731 immune cell traits and a dataset encompassing 895 patients with TB. Subsequently, a cohort including 647 patients with active TB and 632 healthy controls was used to verify the findings of Mendelian randomization (MR). The correlation between the percentage of DP T cells in lymphocytes and TB severity, treatment efficacy, and Mycobacterium tuberculosis (Mtb)-specific IFN-&#x3b3; production was evaluated. Finally, a random forest model incorporating the percentage of DP T cells in leukocytes and other peripheral blood parameters was constructed to distinguish severe from mild active TB. RESULTS: MR analysis suggested potential causal links between the percentage of DP T cells among peripheral leukocytes and TB status. Clinical sample validation showed that the percentage of peripheral DP T cell among leukocytes was significantly lower in patients with active TB than in healthy controls (P < 0.001), and was inversely correlated with disease severity. Additionally, the percentage of DP T cells in leukocytes was positively correlated with Mtb-specific antigen-stimulated IFN-&#x3b3; production. Flow cytometric analysis demonstrated that DP T cells had a significantly higher frequency of IFN-&#x3b3;-expressing cells compared to CD8+ SP T cells (P < 0.001). The constructed random forest model effectively distinguished severe from mild TB, with good diagnostic performance (AUC&#xa0;=&#xa0;0.985). CONCLUSIONS: Our findings indicate that DP T cells are closely associated with TB severity, and are positively associated with Mtb-specific IFN-&#x3b3; response. The percentage of peripheral DP T cells in leukocytes could serve as a potential non-invasive biomarker for TB severity stratification.

Humans