Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1275868 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR33973420_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR33973421_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR33973422_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR33973423_subreads.fastq.gz | Fastqsanger.gz | |||
| SRR33973424_subreads.fastq.gz | Fastqsanger.gz |
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Project description:High cellulose diet aggravates food allergy through gut homeostasis disruption
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Project description:This study investigated the impact of a high cellulose diet (HCD) on intestinal homeostasis and food allergy development in BALB/c mice. While soluble fibers are known to mitigate FA via short-chain fatty acid (SCFA) production, the role of insoluble fibers like cellulose remains unclear. Mice fed HCD exhibited gut dysbiosis, characterized by increased Proteobacteria, decreased tight junction protein expression, and intestinal barrier impairment, despite unchanged SCFA levels. RNA sequencing revealed HCD-induced upregulation of immune pathways, including the positive regulation of B and T cells differentiation and antigen receptor-mediated signaling pathway. Following ovalbumin (OVA) sensitization, HCD-fed mice displayed exacerbated allergic symptoms, including elevated OVA-specific IgE, IgG, histamine, and mMCP-1 levels. Gut microbiota analysis highlighted enrichment of potentially pathogenic taxa in HCD+OVA groups. Fecal microbiota transplantation (FMT) from HCD donors to antibiotic-treated recipients showed severe food allergy responses, confirming microbiota-mediated effects. These findings demonstrate that HCD exacerbates food allergy through gut microbial dysbiosis, intestinal barrier disruption, and intestinal immune disorder.
2025-06-17 | GSE299687 | GEO
Project description:Cutaneous exposure to food antigen through impaired skin barrier has been shown to induce epicutaneous sensitization, and thereby cause IgE-mediated food allergy. We examined whether skin barrier impairment deteriorated food allergy symptoms in epicutaneously sensitized mice. To clarify the association between skin inflammation and food allergy symptoms, we analyzed gene expression at skin lesions using a GeneChip.
2017-06-30 | GSE95278 | GEO
Project description:Oxytocin-expressing paraventricular hypothalamic neurons (PVN^OT neurons) integrate afferent signals from the gut including cholecystokinin (CCK) to adjust whole-body energy homeostasis. However, the molecular underpinnings by which PVN^OT neurons orchestrate gut-to-brain feeding control remain unclear. Here, we show that mice undergoing selective ablation of PVNOT neurons fail to reduce food intake in response to CCK and develop hyperphagic obesity on chow diet. Notably, exposing wildtype mice to a high-fat/high-sugar (HFHS) diet recapitulates this insensitivity towards CCK, which is linked to diet-induced transcriptional and electrophysiological aberrations specifically in PVNOT neurons. Restoring OT pathways in DIO mice via chemogenetics or polypharmacology sufficiently re-establishes CCK?s anorexigenic effects. Lastly, by single-cell profiling, we identify a specialized PVN^OT neuronal subpopulation with increased ?-opioid signaling under HFHS diet, which restrains their CCK-evoked activation. In sum, we here document a novel (patho)mechanism by which PVN^OT signaling uncouples a gut-brain satiation pathway under obesogenic conditions.
2023-09-07 | GSE242245 | GEO
Project description:Food-specific IgE triggers life-threatening anaphylaxis; however, some people with food-specific IgE are asymptomatic upon allergen consumption. Using murine food allergy models, we discovered an unexpected pathway regulating the ability of food allergens to trigger anaphylaxis. C57BL/6 mice are uniquely resistant to anaphylaxis when challenged orally; we show that their gut barrier was impermeable to food allergens relative to anaphylaxis-susceptible strains, even prior to allergic sensitization. In a forward genetic screen, oral anaphylaxis resistance correlated with Dipeptidase1 (Dpep1) allelic variants. DPEP1 is expressed in intestinal epithelium and catabolizes leukotriene D4. Blocking DPEP1 with cilastatin enhanced allergen absorption in resistant mice. Conversely, pre-treatment of susceptible mice with a leukotriene synthesis inhibitor, zileuton, abrogated allergen absorption and subsequent oral anaphylaxis. Inhibiting leukotrienes may be a novel treatment for food allergy.
2025-08-13 | GSE261022 | GEO
Project description:Food-specific IgE triggers life-threatening anaphylaxis; however, some people with food-specific IgE are asymptomatic upon allergen consumption. Using murine food allergy models, we discovered an unexpected pathway regulating the ability of food allergens to trigger anaphylaxis. C57BL/6 mice are uniquely resistant to anaphylaxis when challenged orally; we show that goblet cells transport less food allergens relative to anaphylaxis-susceptible strains, even prior to allergic sensitization. In a forward genetic screen, oral anaphylaxis resistance correlated with Dipeptidase1 (Dpep1) allelic variants. DPEP1 is expressed in intestinal epithelium and catabolizes leukotriene D4 (LTD4). Blocking DPEP1 with cilastatin, genetically deleting Dpep1, or oral administration of LTD4 enhanced allergen transport in resistant mice. Conversely, pre-treatment of susceptible mice with a leukotriene synthesis inhibitor, zileuton, abrogated allergen absorption from the gut and subsequent oral anaphylaxis. Inhibiting leukotrienes may be a novel treatment for food allergy.
2025-08-13 | GSE285568 | GEO
Project description:Tolerance to dietary antigens is critical to avoid deleterious type 2 immune responses resulting in food allergy (FA) and anaphylaxis. However, the mechanisms resulting in both the maintenance and failure of tolerance to food antigens is poorly understood. Here we demonstrate that the goblet cell-derived resistin-like molecule beta (RELMb) is a critical regulator of oral tolerance. We find that RELMb is abundant in serum in both food allergic patients and mouse models of FA. Deletion of RELMβ protects mice from FA, development of food antigen specific IgE and anaphylaxis. RELMb disrupts food tolerance through modulation of the gut microbiome by suppressing gut Lactobacilli. Tolerance is maintained via local production of indole derivatives driving FA protective RORgt+ regulatory T (Treg) cells via activation of the aryl hydrocarbon receptor (AhR). RELMb antagonism in the peri-weaning period restored oral tolerance and protected genetically prone offspring from developing FA later in life. Together, our data identify RELMb as mediating both a novel gut immune-epithelial circuit regulating tolerance to food antigens, a new mode of innate control of antigen specific adaptive immunity via microbiome editing and targetable candidates in this circuit for prevention and treatment of FA.
2022-12-27 | GSE221462 | GEO
Project description:Background: More than 100 million Americans are living with metabolic syndrome, increasing their propensity to develop heart disease– the leading cause of death worldwide. A major contributing factor to this epidemic is caloric excess, often a result of consuming low cost, high calorie fast food. Several recent seminal studies have demonstrated the pivotal role of gut microbes contributing to cardiovascular disease in a diet-dependent manner. Given the central contributions of diet and gut microbiota to cardiometabolic disease, we hypothesized that novel microbial metabolites originating postprandially after fast food consumption may contribute to cardiometabolic disease progression. Methods: To test this hypothesis, we gave conventionally raised or antibiotic-treated mice a single oral gavage of a fast food slurry or a control rodent chow diet slurry and sacrificed the mice four hours later. Here, we coupled untargeted metabolomics in portal and peripheral blood, 16S rRNA gene sequencing, targeted liver metabolomics, and host liver RNA sequencing to identify novel fast food-derived microbial metabolites. Results: We successfully identified several metabolites that were enriched in portal blood, increased by fast food feeding, and essentially absent in antibiotic-treated mice. Strikingly, just four hours post-gavage, we found that fast food consumption resulted in rapid reorganization of the gut microbial community structure and drastically altered hepatic gene expression. Importantly, diet-driven reshaping of the microbiome and liver transcriptome was dependent on a non-antibiotic ablated gut microbial community. Conclusions: Collectively, these data suggest that single fast food meal is sufficient to reshape the gut microbial community yielding a unique signature of food-derived microbial metabolites. Future studies are warranted to determine if these metabolites are causally linked to cardiometabolic disease.
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Project description:This study profiled the epigenomes and transcriptomes of total B cell populations from adolescents with peanut-only (single food allergy- SA) and multi-food allergy (MA).
2021-09-01 | GSE165316 | GEO