Ontology highlight
ABSTRACT:
PROVIDER: PRJNA714090 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR13953325_1.fastq.gz | Fastqsanger.gz | |||
| SRR13953325_2.fastq.gz | Fastqsanger.gz | |||
| SRR13953326_1.fastq.gz | Fastqsanger.gz | |||
| SRR13953326_2.fastq.gz | Fastqsanger.gz | |||
| SRR13953327_1.fastq.gz | Fastqsanger.gz |
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Project description:Probiotic normalization of systemic inflammation in siblings of Type 1 diabetes patients
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Project description:BACKGROUND. The incidence of Type 1 Diabetes (T1D) has significantly increased in recent decades and coincides with lifestyle changes that have likely altered the composition of the gut microbiota. Dysbiosis and gut barrier dysfunction are associated with T1D, and notably, our studies have identified an inflammatory state in T1D families that is consistent microbial antigen exposure. METHODS. We conducted a 6-week, single-arm, open-label trial to investigate whether daily multi-strain probiotic (Bifidobacteria, Lactobacillus, and Streptococcus) supplementation could reduce the familial inflammatory state in 25 unaffected siblings of diabetes patients. RESULTS. Probiotic supplementation was found safe and well-tolerated; there were no adverse events and participant adherence was 93%. Bacterial 16S rDNA gene sequencing of stool revealed that community alpha and beta diversity were not altered between the pre- and post-supplement samplings. LEfSe analyses identified post-supplement enrichment of the family Lachnospiraceae, producers of the anti-inflammatory short chain fatty acid butyrate. Systemic inflammation was measured by plasma induced transcription and quantified with a gene ontology-based composite inflammatory index (I.I.com). After supplementation, I.I.com was reduced (p=0.017), and pathway analysis predicted inhibition of IL17A, lipopolysaccharide, NFkB, IL1B, and TNF (Z-score≤-2.0) and activation of IL10RA (Z-score=2.0). Post-supplement plasma levels of IL12p40, IL-13, IL-15, IL-18, CCL2, CCL24 were reduced (p<0.05), while butyrate levels trended 2.4-fold higher (p=0.06). CONCLUSION. There is a substantial need for safe, broadly applicable therapies to reduce T1D susceptibility. This study indicates that investigations of prebiotic and probiotic strategies are warranted as they may be efficacious either alone or in combination with other therapeutic agents.
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Project description:Periodontitis in elderly patients with type 2 diabetes mellitus: impact on gut microbiota and systemic inflammation
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Project description:Obesity-induced adipose tissue dysfunction can cause low-grade inflammation and downstream obesity comorbidities. Although preadipocytes may contribute to this pro-inflammatory environment, the underlying mechanisms are unclear. We used human primary preadipocytes from body mass index (BMI) -discordant monozygotic (MZ) twin pairs to generate epigenetic (ATAC-sequence) and transcriptomic (RNA-sequence) data for testing whether increased BMI alters the subnuclear compartmentalization of open chromatin in the twins’ preadipocytes, causing downstream inflammation. Here we show that the co-accessibility of open chromatin, i.e. compartmentalization of chromatin activity, is altered in the higher vs lower BMI MZ siblings for a large subset (~88.5Mb) of the active subnuclear compartments. Using the UK Biobank we show that variants within these regions contribute to systemic inflammation through interactions with BMI on C-reactive protein. In summary, open chromatin co-accessibility in human preadipocytes is disrupted among the higher BMI siblings, suggesting a mechanism how obesity may lead to inflammation via gene-environment interactions.
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Project description:Systemic inflammation is reported to be associated with neutrophilic airway inflammation in asthma, this study aimed to examine the molecular mechanisms of the neutrophilia that is associated with systemic inflammation, and hypothesized that asthma patients with systemic inflammation have a group of genes that are differentially expressed and are assciated with airway inflammation. 50 asthma patients were recruited and grouped as asthmatics with systemic inflammation (n=18) and asthamtics without systemic inflammation (n=16) accroding to the levels of serum CRP and IL-6. RNA was extracted from induced sputum and was reverse-transcribed into cDNA. Gene profiling was performed using Illumina Sentrix HumanRef-8 Version 2 Expression BeadChips, and genes that were differentially expressed between asthmatics with systemic inflammation and asthmatics without systemic inflammation were compared and valided using qPCR.
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Project description:The most abundant and central component, glycoprotein C3, contributes to the development of type 1 diabetes by enhancing the organ-specific autoimmune inflammatory processes. It is known that changes in glycosylation can modulate inflammatory responses and we recently showed that children at the onset of type 1 diabetes have a higher proportion of oligomannose glycans in plasma N-glycome compared to their healthy siblings. Due to fact that C3 contains two N-glycosylation sites occupied by this type of glycans, our aim was to develop a novel high-throughput and cost-effective glycoproteomic workflow for N-glycosylation analysis of human C3 to reveal the possible role of C3 glycosylation in type 1 diabetes development.
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Project description:The most abundant and central component, glycoprotein C3, contributes to the development of type 1 diabetes by enhancing the organ-specific autoimmune inflammatory processes. It is known that changes in glycosylation can modulate inflammatory responses and we recently showed that children at the onset of type 1 diabetes have a higher proportion of oligomannose glycans in plasma N-glycome compared to their healthy siblings. Due to fact that C3 contains two N-glycosylation sites occupied by this type of glycans, our aim was to develop a novel high-throughput and cost-effective glycoproteomic workflow for N-glycosylation analysis of human C3 to reveal the possible role of C3 glycosylation in type 1 diabetes development.
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Project description:Type 1 diabetes (T1D) is an autoimmune disease characterized by destruction of the pancreatic β-cells. T1D pathogenesis has a strong genetic basis. However, in recent decades, the prevalence of high-risk HLA haplotypes among new diagnoses has declined, the age of onset has decreased, and T1D incidence has increased. These changes are consistent with increased environmental pressure and coincide with introduction of the Western diet, widespread antibiotic use and reduced breast feeding. These factors are thought to drive intestinal dysbiosis, increased gut permeability and systemic inflammation. Notably, our studies of T1D families and the BioBreeding (BB) rat have identified a peripheral inflammatory state associated with diabetes susceptibility that is consistent with microbial antigen exposure and pattern recognition receptor ligation. Lactiplantibacillus plantarum 299v (Lp299v), a probiotic strain, is reported to increase plasma and stool levels of anti-inflammatory short chain fatty acids (SCFA) and promote IL-10 signaling in colonic derived macrophages and T-cells. Here we investigated the effect of Lp299v supplement on T1D progression and inflammatory phenotypes in diabetes prone BB DRlyp/lyp rats. Rats were weaned at 21 days onto a normal cereal diet (ND) or a gluten-free hydrolyzed casein diet (HCD), with and without daily Lp299v supplementation. All DRlyp/lyp ND rats developed T1D by day 83 (mean time to onset of 62.8+/-7.9 days). DRlyp/lyp ND+Lp299v rats exhibited an insignificant delay in T1D onset (62.6+/-6.5 days), however 8% remained diabetes-free to day 130. Providing DRlyp/lyp rats HCD prevented T1D in 17% of rats (to age 130 days) and significantly delayed onset (mean time to onset 72.8+/-7.3 days, p<0.001). Providing DRlyp/lyp rats HCD+Lp299v prevented T1D in 25% of rats and more robustly delayed onset (mean time to onset 84.9 +/-14.3 days, p<0.001). While multiplex ELISA failed to detect significantly altered plasma cytokine/chemokine levels at 40 days of life, plasma induced transcription revealed greatest normalization of systemic inflammation in the HCD+Lp299v group. Plasma SCFA levels (propionate and butyrate, p<0.01) were elevated in the HCD+Lp299v group compared to the ND group. Global gene expression analysis of pancreatic islets was conducted at 40 days, prior to insulitis. Endoplasmic reticulum (ER) stress has been implicated in the formation of islet neoantigens that may underlie the initial loss of immune tolerance in T1D. Under one or both diets, Lp299v favorably modulated islet expression levels of pathways and transcripts related to inflammation and innate immunity (Cxcl9, Cxcl10), oxidative stress (Gsta1, Gsta4, Gstp1, Gstk1), as well as ER stress and unfolded protein response (Cirbp, Edem1, Hspa1a, Atf4). These ongoing studies add to a growing understanding that inherited susceptibility can be modulated by diet and microbiota.
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