Ontology highlight
ABSTRACT:
PROVIDER: PRJNA484972 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7657450_1.fastq.gz | Fastqsanger.gz | |||
| SRR7657450_2.fastq.gz | Fastqsanger.gz | |||
| SRR7657460_1.fastq.gz | Fastqsanger.gz | |||
| SRR7657460_2.fastq.gz | Fastqsanger.gz | |||
| SRR7657470_1.fastq.gz | Fastqsanger.gz |
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Project description:Dysbiotic microbiome triggers Th17 cells to mediate oral mucosal immunopathology in mice and humans
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Project description:Animal model implicates microbiota-triggered oral mucosal Th17 cells as drivers of local immunopathology and therapeutic targets in periodontitis.
2018-12-31 | GSE118166 | GEO
Project description:At mucosal surfaces, epithelial cells provide a structural barrier and an immune defense system. However, dysregulated epithelial responses can contribute to disease states. Here, we demonstrate that epithelial intrinsic production of IL-23 triggers an inflammatory loop in the prevalent oral disease, periodontitis. Epithelial IL-23 expression localized to areas proximal to the disease-associated microbiome, is evident both in experimental models and in patients with common and genetic forms of disease. Mechanistically, flagellated microbial species of the periodontitis microbiome, trigger epithelial IL-23 induction in a TLR5-dependent manner. Intriguingly, unlike other Th17-driven diseases, here non-hematopoietic cell-derived IL-23 serves as an initiator of pathogenic inflammation. Beyond periodontitis, analysis of publicly available datasets reveals expression of epithelial IL-23 in settings of infection, malignancy, and autoimmunity, suggesting a broader role for epithelial-intrinsic IL-23 in human disease. Collectively, this work highlights an unappreciated role for the barrier epithelium in the induction of IL-23-mediated inflammation.
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Project description:Plasminogen (Plg), the zymogen precursor of the serine protease plasmin, is synthesized by the liver and is present in high concentration in the circulation and in interstitial fluids to provide focal proteolysis, after being converted to plasmin by urokinase or tissue plasminogen activator. Homozygous or compound heterozygous mutations in the human Plg gene (PLG) typically lead to severe mucosal disease involvement suggesting, a critical role for this gene/pathway in mucosal immunity. Indeed, such patients present with deposition of fibrin at various mucosal sites leading to ocular disease (conjunctivitis), oral mucosal disease (ligneous periodontitis), lung, vaginal and gastrointestinal tract involvement. In the oral mucosa, local deposition of fibrin is hypothesized to lead to severe soft tissue and bone destruction around teeth and often loss of the entire dentition in adolescence. Mucosal inflammation in areas surrounding the dentition and destruction of underlying bone are also the hallmarks of the common human oral mucosal disease, periodontitis. Plg-deficient mice phenocopy the human disease and we aim to use this animal model to understand the mechanism underlying fibrin-mediated periodontal immunopathology in vivo. Herein, we analyse the transcriptome of gingival tissues extracted from Plg-deficient mice in comparison to their wild-type littermates at 12 weeks of age.
2022-06-02 | GSE178616 | GEO
Project description:The development of neutralizing FVIII antibodies is the most serious complication of hemophilia A treatment. The currently known patient- and treatment-related risk factors for inhibitor development do not accurately predict this adverse event in all patients. The composition of the gut microbiota has been shown to influence immune mediated diseases at distant anatomical sites (e.g. lungs, brain and joints). We demonstrate that a disrupted gut microbiome can be created in a mouse model of hemophilia A using a broad-spectrum antibiotic. Under controlled conditions, this sustained dysbiosis was associated with an enhanced anti-FVIII immune response as evidenced by increased splenic B cells and the development of higher titre FVIII specific IgG antibodies following FVIII challenge. Splenic and mesenteric lymph node cytokines, T cells and dendritic cells were unaffected prior to FVIII administration. However, the immune transcriptome of both aforementioned secondary lymphoid organs was significantly modified. Short chain fatty acids (SCFA), which are microbial metabolites, were depleted in cecal contents of the dysbiotic mice. Furthermore, supplementation of the drinking water with the most immunologically active SCFA, butyrate, successfully achieved attenuation of the FVIII immune response. Collectively, our data suggest that the composition of the gut microbiome alters the FVIII immune response via the action of specific microbial metabolites on the immune cell transcriptome and that oral butyrate supplementation effectively reduces the FVIII immune response. Mice treated with one week of ampicillin at 3 weeks of age have a dysbiotic gut microbiome at 6 weeks of age and at the study endpoint. The immune response to FVII was compared between the two cohorts. The dysbiotic cohort had a greater immune response to FVIII
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Project description:Leber2015 - Mucosal immunity and gut
microbiome interaction during C. difficile infection
This model is described in the article:
Systems Modeling of
Interactions between Mucosal Immunity and the Gut Microbiome
during Clostridium difficile Infection.
Leber A, Viladomiu M, Hontecillas R,
Abedi V, Philipson C, Hoops S, Howard B, Bassaganya-Riera
J.
PLoS ONE 2015; 10(7): e0134849
Abstract:
Clostridium difficile infections are associated with the use
of broad-spectrum antibiotics and result in an exuberant
inflammatory response, leading to nosocomial diarrhea, colitis
and even death. To better understand the dynamics of mucosal
immunity during C. difficile infection from initiation through
expansion to resolution, we built a computational model of the
mucosal immune response to the bacterium. The model was
calibrated using data from a mouse model of C. difficile
infection. The model demonstrates a crucial role of T helper 17
(Th17) effector responses in the colonic lamina propria and
luminal commensal bacteria populations in the clearance of C.
difficile and colonic pathology, whereas regulatory T (Treg)
cells responses are associated with the recovery phase. In
addition, the production of anti-microbial peptides by inflamed
epithelial cells and activated neutrophils in response to C.
difficile infection inhibit the re-growth of beneficial
commensal bacterial species. Computational simulations suggest
that the removal of neutrophil and epithelial cell derived
anti-microbial inhibitions, separately and together, on
commensal bacterial regrowth promote recovery and minimize
colonic inflammatory pathology. Simulation results predict a
decrease in colonic inflammatory markers, such as neutrophilic
influx and Th17 cells in the colonic lamina propria, and length
of infection with accelerated commensal bacteria re-growth
through altered anti-microbial inhibition. Computational
modeling provides novel insights on the therapeutic value of
repopulating the colonic microbiome and inducing regulatory
mucosal immune responses during C. difficile infection. Thus,
modeling mucosal immunity-gut microbiota interactions has the
potential to guide the development of targeted fecal
transplantation therapies in the context of precision medicine
interventions.
This model is hosted on
BioModels Database
and identified by:
BIOMD0000000583.
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BioModels Database:
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To the extent possible under law, all copyright and related or
neighbouring rights to this encoded model have been dedicated to
the public domain worldwide. Please refer to
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2024-09-02 | BIOMD0000000583 | BioModels
Project description:The development of neutralizing FVIII antibodies is the most serious complication of hemophilia A treatment. The currently known patient- and treatment-related risk factors for inhibitor development do not accurately predict this adverse event in all patients. The composition of the gut microbiota has been shown to influence immune mediated diseases at distant anatomical sites (e.g. lungs, brain and joints). We demonstrate that a disrupted gut microbiome can be created in a mouse model of hemophilia A using a broad-spectrum antibiotic. Under controlled conditions, this sustained dysbiosis was associated with an enhanced anti-FVIII immune response as evidenced by increased splenic B cells and the development of higher titre FVIII specific IgG antibodies following FVIII challenge. Splenic and mesenteric lymph node cytokines, T cells and dendritic cells were unaffected prior to FVIII administration. However, the immune transcriptome of both aforementioned secondary lymphoid organs was significantly modified. Short chain fatty acids (SCFA), which are microbial metabolites, were depleted in cecal contents of the dysbiotic mice. Furthermore, supplementation of the drinking water with the most immunologically active SCFA, butyrate, successfully achieved attenuation of the FVIII immune response. Collectively, our data suggest that the composition of the gut microbiome alters the FVIII immune response via the action of specific microbial metabolites on the immune cell transcriptome and that oral butyrate supplementation effectively reduces the FVIII immune response. Mice treated with one week of ampicillin at 3 weeks of age have a dysbiotic gut microbiome throughout the study and an enhanced immune response to FVIII which was administered at 6 weeks of age. Here we assess the immune transcriptome in the mice spleen and Mesenteric lymph nodes at 6 weeks of age, just prior to exposure to FVIII challenge.
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Project description:Citrobacter rodentium is commonly used to elucidate mucosal responses to infection in mice developing mild disease (e.g. C57BL/6), while little is known about host responses to infection in mice developing severe disease (e.g. C3H/HeN). We report that the phyla Bacteroidetes is a minor component of the tissue-associated microbiome in uninfected C3H/HeN mice. Following infection, C. rodentium rapidly and uniformly colonises the C3H/HeN colonic mucosa, which coincides with downregulation of proteins involved in the TCA cycle and oxidative phosphorylation in intestinal epithelial cells (IECs). In contrast, we observed upregulation of DNA replication and DNA damage repair processes, as well as cholesterol biogenesis, import and export, nutritional immunity, IL-22 and INFg responses, and expression of NLRP3, in IECs. Moreover, C. rodentium triggers a staggered cell proliferation response from 3 days post infection, which correlated with a higher abundance of SLC5A9 and reduced abundance of the IEC differentiation markers SLC26A3 and CA4. Uniquely, C. rodentium triggers differential secretion of gel-forming mucins, with the number of goblet cells filled with acidic and neutral mucins dramatically increasing and decreasing, respectively. Together, these results show that despite vigorous responses, C3H/HeN mice succumb to C. rodentium infection, possibly as a result of excessive and disordered mucosal responses.
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