Akkermansia muciniphila regulates food allergy in a diet-dependent manner
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB53451 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR11730100_1.fastq.gz | Fastqsanger.gz | |||
| ERR11730100_2.fastq.gz | Fastqsanger.gz | |||
| ERR11730101_1.fastq.gz | Fastqsanger.gz | |||
| ERR11730101_2.fastq.gz | Fastqsanger.gz | |||
| ERR11730102_1.fastq.gz | Fastqsanger.gz |
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Project description:Alterations in the gut microbiome, including diet-driven changes, are linked to the rising prevalence of food allergy. However, little is known about how specific gut bacteria trigger the breakdown of oral tolerance. Here we show that depriving specific-pathogen-free mice of dietary fibre leads to a gut microbiota signature with increases in the mucin-degrading bacterium Akkermansia muciniphila. This signature is associated with intestinal barrier dysfunction, increased expression of type 1 and 2 cytokines and IgE-coated commensals in the colon, which result in an exacerbated allergic reaction to food allergens, ovalbumin and peanut. To demonstrate the causal role of A. muciniphila, we employed a tractable synthetic human gut microbiota in gnotobiotic mice. The presence of A. muciniphila within the microbiota, combined with fibre deprivation, resulted in stronger anti-commensal IgE coating and innate type-2 immune responses, which worsened symptoms of food allergy. Our study provides important insights into how gut microbes can regulate immune pathways of food allergy in a diet-dependent manner.
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Project description:The erosion of the colonic mucus layer by a dietary fiber-deprived gut microbiota results in heightened susceptibility to an attaching and effacing pathogen, Citrobacter rodentium. Nevertheless, the questions of whether and how specific mucolytic bacteria aid in the increased pathogen susceptibility remain unexplored. Here, we leverage a functionally characterized, 14-member synthetic human microbiota in gnotobiotic mice to deduce which bacteria and functions are responsible for the pathogen susceptibility. Using strain dropouts of mucolytic bacteria from the community, we show that Akkermansia muciniphila renders the host more vulnerable to the mucosal pathogen during fiber deprivation. However, the presence of A. muciniphila reduces pathogen load on a fiber-sufficient diet, highlighting the context-dependent beneficial effects of this mucin specialist. The enhanced pathogen susceptibility is not owing to altered host immune or pathogen responses, but is driven by a combination of increased mucus penetrability and altered activities of A. muciniphila and other community members. Our study provides novel insights into the mechanisms of how discrete functional responses of the same mucolytic bacterium either resist or enhance enteric pathogen susceptibility.
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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:This study profiled the epigenomes and transcriptomes of total nCD4T cell populations from adolescents with peanut-only (single food allergy- SA) and multi-food allergy (MA) at quiescence and following activation with anti-CD3/antiCD28
2022-02-28 | GSE189148 | GEO
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).
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Project description:Background: The prevalence of individuals allergic to latex, exhibiting cross-hypersensitivity with plant-derived food has been frequently reported as the so-called latex-fruit syndrome. Nonetheless, molecular mechanisms underlying allergy to latex and/or fruit are poorly understood. Objective: The aims of this study were to identify candidate genes that may be associated with the pathogenesis of allergy to latex and /or vegetable food, and to assess if similar molecular pathways are involved in both types of hypersensitivity. Methods: DNA microarray analysis was performed to screen the molecular profiles of peripheral blood mononuclear cells isolated from patients with allergy to latex, to fruit, or with latex-fruit syndrome, and from control healthy subjects. Results: Gene expression profiling identified an overlapping dataset of genes commonly regulated in all the atopic patients enrolled in this study, suggesting that similar molecular mechanisms are involved in the pathogenesis of allergy to the fruit and /or latex. Several regulators of the innate and acquired immunity reported to polarize the immunological response towards a Th2-mediated immune response were overexpressed in patients. Furthermore, evidences suggested that T regulatory cell expression might be defective in allergic patients, as a consequence of a dysregulation of some inflammatory cytokines. Finally, several transcription factors that may be responsible for the Th1/Th2 imbalance were modulated in allergic patients. Conclusion and clinical implications: This study identified relevant genes that may help to elucidate the molecular mechanisms underlying allergic disease. Knowledges of critical targets, along with transcription factors regulating gene activity may facilitate the development of new therapies. Experiment Overall Design: This study aimed at the understanding of the molecular pathways involved in allergy to latex and fruit. As latex and vegetable food allergens cross-react, it could be hypothesized that similar pathways are involved in both types of hypersensitivity. Experiment Overall Design: For this purpose, patients allergic to latex (n=6), allergic to vegetable food (n=5), or suffering from latex-fruit syndrome (n=6) were enrolled from the Unit of Allergy of the Gemelli Hospital of Rome. Moreover, 4 healthy volunteers were added to this study. Five ml of blood were harvested from each individual, and PBMCs were isolated on ficoll gradient. Following sample preparation (as recommended by the manufacturer), each sample was hybridized on Affymetrix human focus array. Data were processed with Affymetrix MAS 5.0 software and averaged intensity of signals from biological replicates were calculated for further analysis. Experiment Overall Design: The CEL files for this study were lost in a computer crash.
2009-08-09 | E-GEOD-13619 | biostudies-arrayexpress
Project description:Experimental IgE-mediated food allergy depends on intestinal anaphylaxis driven by interleukin (IL)-9. However, the primary cellular source of IL-9 and the mechanisms underlying the susceptibility to food-induced intestinal anaphylaxis remain unclear. Herein, we have reported the identification of multifunctional IL-9-producing mucosal mast cells (MMC9s) that can secrete prodigious amounts of IL-9 and IL-13 in response to IL-33, and mast cell protease-1 (MCPt-1) in response to antigen and IgE complex crosslinking, respectively. Repeated intragastric antigen challenge induced MMC9 development that required T cells, IL-4, and STAT6 transcription factor, but not IL-9 signals. Mice ablated of MMC9 induction failed to develop intestinal mastocytosis, which resulted in decreased food allergy symptoms that could be restored by adoptively transferred MMC9s. Finally, atopic patients that developed food allergy displayed increased intestinal expression of Il9 and MC-specific transcripts. Thus, the induction of MMC9s is a pivotal step to acquire the susceptibility to IgE-mediated food allergy. dUTP mRNA-Seq profiles of indicated hematopoietic cell lineages were generated on Illumina HiSeq2500. Hematopoietic cells were isolated from Balb/C mice that developed food allergy and bone marrow-derived mast cells were generated from naïve Balb/C mice
2015-09-11 | E-GEOD-72921 | biostudies-arrayexpress
Project description:This study profiled the epigenomes and transcriptomes of total nCD4T cell populations from adolescents with peanut-only (single food allergy- SA) and multi-food allergy (MA) at quiescence and following activation with anti-CD3/antiCD28
2022-02-28 | GSE189149 | GEO
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). We found distinct epigenetic and transcriptomic differences between food allergic patients and controls, in addition to SA- and MA- group specific signatures, with
2021-09-01 | GSE166067 | GEO
Project description:Obesity and type 2 diabetes are characterized by altered gut microbiota, inflammation, and gut barrier disruption. Microbial composition and the mechanisms of interaction with the host that affect gut barrier function during obesity and type 2 diabetes have not been elucidated. We recently isolated Akkermansia muciniphila, which is a mucin-degrading bacterium that resides in the mucus layer. The presence of this bacterium inversely correlates with body weight in rodents and humans. However, the precise physiological roles played by this bacterium during obesity and metabolic disorders are unknown. This study demonstrated that the abundance of A. muciniphila decreased in obese and type 2 diabetic mice. We also observed that prebiotic feeding normalized A. muciniphila abundance, which correlated with an improved metabolic profile. In addition, we demonstrated that A. muciniphila treatment reversed high-fat diet-induced metabolic disorders, including fat-mass gain, metabolic endotoxemia, adipose tissue inflammation, and insulin resistance. A. muciniphila administration increased the intestinal levels of endocannabinoids that control inflammation, the gut barrier, and gut peptide secretion. Finally, we demonstrated that all these effects required viable A. muciniphila because treatment with heat-killed cells did not improve the metabolic profile or the mucus layer thickness. In summary, this study provides substantial insight into the intricate mechanisms of bacterial (i.e., A. muciniphila) regulation of the cross-talk between the host and gut microbiota. These results also provide a rationale for the development of a treatment that uses this human mucus colonizer for the prevention or treatment of obesity and its associated metabolic disorders.
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