Sex drives colonic mucin sialylation in wild mice - RNAseq
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB68152 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR12195466_1.fastq.gz | Fastqsanger.gz | |||
| ERR12195466_2.fastq.gz | Fastqsanger.gz | |||
| ERR12195467_1.fastq.gz | Fastqsanger.gz | |||
| ERR12195467_2.fastq.gz | Fastqsanger.gz | |||
| ERR12195468_1.fastq.gz | Fastqsanger.gz |
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Project description:Following observations that sex of wild animals is associated with the acidity of colonic mucin glycans, as determined via histology, RNA sequencing was undertaken to explore potential mechanisms driving these differences. Colonic tissue samples from 24 male mice trapped on the Isle of May in October 2019 were selected, encompassing a range of staining profiles, following Alcian Blue PAS staining of colonic tissue. Using IPA software Esr1 signalling was identified as the major upstream regulator of gene expression associated with varied mucin acidity.
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Project description:Chronic infection of the lungs by bacteria such as Pseudomonas aeruginosa plays an important role in the natural history of Cystic Fibrosis (CF). Altered mucin secretions and glycosylations are hallmarks of bacterial infections but their exact contributions to the development of chronic infection and/or inflammation remain to be established. We studied the lung environment in newborn CFTR-/- pigs, which closely mirrors the human CF phenotype at the levels of mucin glycosylation, mucociliary transport (MCT) and immune response to P. aeruginosa infections. We show an increased sialylation of mucins from the tracheal mucosa of CFTR-/- pigs, which is also associated to increased Pseudomonas aeruginosa adherence. RNA-seq analysis did not show any altered expression of inflammatory genes, nor of sialylation enzymes. CFTR-/- piglets were unable to clear P. aeruginosa from the airways, leading to increased bacteria time of residence in the airways. We propose that alterations in mucin sialylation and MCT directly contribute to the early development of a favorable environment for bacterial colonization of the CF airways in the absence of an intrinsic inflammation.
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Project description:B3GNT7, an important glycosyltransferase highly expressed in intestinal epithelial cells, is involved in physiological processes in the intestine. This study presents novel findings on the potential role and mechanism of B3GNT7 in ulcerative colitis (UC). DSS-induced mouse model of colitis was established to investigate the expression of B3GNT7 in the colon using transcriptomics and immunohistochemistry. Bioinformatics analysis was conducted to explore the biological functions of B3GNT7. The correlation between the transcription levels of B3GNT7 in the colonic tissues of UC patients from the IBDMDB database was analyzed and the severity of colonic inflammation, along with potential mechanisms. The DSS-induced colitis mouse model was successfully established, and transcriptomic analysis revealed a significant downregulation of B3GNT7 expression in the colonic tissues compared to healthy mice. Functional enrichment analysis showed that the main biological function of B3GNT7 was to participate in the mucin O-glycosylation process. Protein interaction analysis indicates that the molecules showing strong interaction with B3GNT7 were members of the mucin MUC family, including MUC2, MUC3, and MUC6. In UC patients, the transcription levels of B3GNT7 were significantly decreased, particularly in patients with moderate to severe disease activity. The expression level of B3GNT7 was negatively correlated with the endoscopic severity of UC. Gene set enrichment analysis (GSEA) further revealed significant enrichment of B3GNT7 in the mucin O-glycosylation synthesis signaling pathway. The downregulation of B3GNT7 expression in the colonic tissues of UC may contribute to impaired mucin barrier function and the progression of colitis.
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Project description:The human gut microbiota is crucial for degrading dietary fibres from the diet. However, some of these bacteria can also degrade host glycans, such as mucins, the main component of the protective gut mucus layer. Specific microbiota species and mucin degradation patterns are associated with inflammatory processes in the colon. Yet, it remains unclear how the utilization of mucin glycans affects the degradation of dietary fibres by the human microbiota. Here, we used three dietary fibres (apple pectin, β-glucan and xylan) to study in vitro the dynamics of colon mucin and dietary fibre degradation by the human faecal microbiota. The dietary fibres showed clearly distinguishing modulatory effects on faecal microbiota composition. The utilization of colon mucin in cultures led to alterations in microbiota composition and metabolites. Metaproteome analysis showed the central role of the Bacteroides in degradation of complex fibres while Akkermansia muciniphila was the main degrader of colonic mucin. This work demonstrates the intricacy of complex glycan metabolism by the gut microbiota and how the utilization of host glycans leads to alterations in the metabolism of dietary fibres. Metaproteomics analysis of this data reveals the functional activities of the bacteria in consortia, by this contributing to a better understanding of the complex metabolic pathways within the human microbiota that can be manipulated to maximise beneficial microbiota-host interactions. In this study two different mucin samples were used: commercial porcine gastric mucin and in house prepared porcine colonic mucin. This dataset analyses the proteome of: A) autoclaved porcine colonic mucin; B) not autoclaved porcine colonic mucin; C) porcine gastric mucin.
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Project description:Immunoglobulin G (IgG) Fc glycosylation critically regulates antibody effector functions, yet the pathogenic potential of early glycoform dynamics during acute viral infection remains poorly understood. Here, we identify a transient enrichment of sialylated IgG (Sia-IgG) during the early phase of SARS-CoV-2 infection that acts as a key driver of lung immunopathology. Contrary to the conventional anti-inflammatory role of sialylation, early-phase Sia-IgG fails to confer protection upon secondary viral challenge and instead aggravates lung injury despite reduced viral burden. Single-cell transcriptomic analysis of COVID-19 lungs reveals a selectively expanded SIGLEC1⁺ monocyte-derived macrophage population as a potential cellular target of this pathogenic signaling. Functional assays show that acute-phase IgG drives macrophage inflammatory infiltration in an FcγR-dependent manner. Moreover, acute-phase serum impairs phagocytic capacity and downregulates expression of the homeostatic marker CD206 in macrophages, indicative of a phenotypic shift toward a pro-inflammatory, dysfunctional state. Mechanistically, Sia-IgG coordinates the synergistic engagement of Siglec-1 and FcγRs, triggering mitochondrial immunometabolic collapse via VDAC1 oligomerization, excessive mitochondrial reactive oxygen species production, and impaired oxidative phosphorylation. Collectively, our findings define pathogenic IgG sialylation as a critical determinant of macrophage reprogramming, establishing a Siglec-1-FcγR-VDAC1 signaling axis that links humoral glycomic shifts to severe respiratory immunopathology during viral infection.
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Project description:Breast cancer is the most prevalent cancer among women, yet immune checkpoint inhibitors remain largely ineffective in the majority of patients. To better understand the mechanisms underlying immune evasion in breast cancer, we analyzed two independent clinical cohorts and identified a negative association between tumor sialylation and T cell infiltration across molecular subtypes, most prominently in luminal B tumors. In preclinical models, both genetic and pharmacologic inhibition of tumor cell sialylation reshape the tumor microenvironment by reducing neutrophil and PMN-MDSC infiltration, while CD8⁺ effector and Tcf7⁺ memory T cells are increased within the mammary tumors. Mechanistically, sialylation enhances the serum half-life of granulocyte colony-stimulating factor (G-CSF), a key driver of neutrophilic immunosuppression, and dampens tumor cell immunogenicity by limiting MHC-I surface expression. Disruption of sialylation sensitizes resistant mammary tumors to CD8⁺ T cell-mediated killing and synergizes with anti-PD-1 therapy in multiple breast cancer models. Analysis of patient datasets further reveals a sialylation gene signature enriched in breast tumors, especially of the luminal B subtype, that correlates with increased neutrophils and poor CD8⁺ T cell infiltration. Our findings establish tumor cell sialylation as a central regulator of immune evasion in breast cancer, offering a therapeutic vulnerability to unlock anti-tumor immunity and improve responsiveness to immune checkpoint inhibitors.
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Project description:Multiple Sclerosis (MS) is a chronic autoimmune disease that targets the myelin sheath of the central nervous system (CNS), with a higher prevalence in female patients. Our previous works demonstrated a bidirectional link between the gut microbiota and experimental autoimmune encephalomyelitis (EAE), a rodent model of MS. In this study, we aimed to assess sex as a biological variable in the host and microbiota colonic microenvironment at early and late stages of neuroinflammation. A combination of two independent experiments showed no significant differences between male and female C57BL/6J mice in the EAE incidence, disease onset, and disease severity. We performed colonic transcriptomics and microbiota analysis in colonic fecal content of EAE mice and controls on the day of disease induction, pre-onset, and peak disease (seven mice per group/times). Our transcriptomics analysis revealed significant sex-specific differences in colonic gene expression during EAE. Notably, at peak disease, these pathways involved a small number of crucial genes. Similarly, significant effects on the gut microbiota of female and male mice were observed by 16S rRNA amplicon sequencing. We also report a novel visualization tool that combines transcriptomics and microbiome sequencing data that allows sex-dependent and disease stage-dependent clustering. Our findings suggest the involvement of critical inflammatory pathways during the early stages of the disease, with remarkable differences between males and females associated with microbiota alterations triggered by disease induction and progression.
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Project description:Background: Ulcerative colitis (UC) develops from chronic inflammation of the colon. Most patients respond favorably to medical management, however around 25% of UC patients will require surgery to treat their disease. While surgery is the only curative treatment for UC, it can carry its own risks, particularly when the surgery is emergent. Time from diagnosis to surgery varies dramatically amongst UC patients, thus a better understanding of how the colonic microenvironment relates to disease severity is needed to improve patient outcomes. Methods: We conducted RNA-seq on full-thickness sigmoid colonic tissues from 26 UC patients undergoing colectomy for their disease. Hierarchical clustering of the transcriptomes identified disease subsets. Subsets were characterized using differential gene expression analysis, cell type deconvolution, and network analysis. Results: We identified two distinct UC subsets in our cohort that were distinguished by 957 differentially expressed genes. Cluster 1 was enriched in genes associated with intestinal epithelial cell differentiation, while cluster 2 was enriched in genes associated with epithelial-to-mesenchymal transition and inflammatory responses. Cluster 1 was associated with an extended time from UC diagnosis to colectomy. Of cluster 1 genes, elevated MUC5B, MUC4, and MUC2 expression displayed the strongest correlation with increased time to surgery. Conclusion: Our transcriptome analysis indicates that UC can be subclassified into at least two distinct molecular signatures. We find that elevated mucin gene expression correlates with prolonged time to colectomy after diagnosis. These results identified MUC5B, MUC4, and MUC2 as potential prognostic indicators of disease severity, as reflected in time to surgery.
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