Colonic lavage samples
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA737297 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Colonic aspirates were collected at diagnostic colonoscopy from inflammatory bowel disease (IBD) and control, treatment-naive children. The colonic mucosal-luminal interface (MLI) proteomes were analyzed for 18 control and 42 IBD patients by liquid-chromatography mass spectrometry.
2018-03-19 | PXD006383 | Pride
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.
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2014-04-08 | BIOMD0000000583 | BioModels
Project description:Virome sequencing of the human colonic mucosal-luminal interface
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Project description:Transcriptional profiling of microscopically laser dissected murine colonic tissue from 3 separate normal crypts, wound associated epithelium (WAE), normal epithelium, and regenerating crypts (day 6 only) at days 2,4,and 6 after colonic mucosal injury. Injury model performed as described in: H. Seno et al., Efficient colonic mucosal wound repair requires Trem2 signaling. Proc. Natl. Acad. Sci. USA 106, 256-261 (2009)
2012-06-18 | E-MTAB-1175 | biostudies-arrayexpress
Project description:Colonic mucosal injury responses
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Project description:Colonic epithelial cells facilitate host-microbe interactions to control mucosal immunity, and they also coordinate recycling and forming the mucus barrier. Epithelial barrier breakdown underpins inflammatory bowel disease (IBD). However, we do not know the specific contributions of each epithelial cell subtype to this process. Here, we profiled single colonic epithelial cells in health and IBD. Our results identified previously unknown subtypes and crypt gradients of progenitors, colonocytes and goblet cells. We also revealed a novel specialized metal ion storage and chloride secretory cell. In IBD, we discovered a unique cluster of disease associated goblet cells that remodels the barrier. We found downregulated WFDC2, a novel goblet cell expressing anti-protease that inhibited bacterial growth. Our in vivo studies demonstrated WFDC2 preserved tight junction integrity and prevented commensal invasion and mucosal inflammation. We delineate markers and transcriptional states, identify a new colonic epithelial cell and uncover fundamental principles of epithelial plasticity and barrier breakdown in IBD. Thus, our study reveals new therapeutic targets and disease-related mechanisms in IBD
2019-02-16 | PXD011655 | Pride
Project description:The intestinal epithelium is a key physical interface that integrates dietary and microbial signals to regulate nutrient uptake and mucosal homeostasis. Intestinal epithelial cells (IECs) have a high turnover rate driven by the death of terminally differentiated cells with concurrent stem cell proliferation, a process critical for maintaining intestinal homeostasis and protecting against mucosal inflammation. The transcriptional programs that regulate IEC quiescence, proliferation, and differentiation have been well-characterized. However, how gene expression networks critical for IEC functions are regulated at the post-transcriptional level during homeostasis or inflammatory disease remains poorly understood. Herein, we show that a conserved family of microRNAs, miR-181, is significantly downregulated in IECs from patients with inflammatory bowel disease and mice with chemical-induced colitis. Strikingly, we showed that miR-181 expression within IECs, but not the hematopoietic system, is required for protection against the development of severe colonic inflammation in response to epithelial injury in mice. Mechanistically, we showed that miR-181 expression increases the proliferative capacity of IECs, likely through the regulation of Wnt signaling, independently of gut microbiota composition. As epithelial reconstitution is crucial for restoring intestinal homeostasis after injury, the miR-181 family represents a potential novel therapeutic target in IECs for protection against severe intestinal inflammation.
2022-07-25 | GSE208410 | GEO
Project description:How pathogenesis of inflammatory bowel disease (IBD) depends on the complex interplay of host genetics, microbiome and the immune system is not fully understood. Here, we showed that Downstream of Kinase 3 (DOK3), an adaptor protein involved in immune signaling, confers protection of mice from dextran sodium sulfate (DSS)-induced colitis. DOK3-deficiency promotes gut microbial dysbiosis and enhanced colitis susceptibility, which can be reversed by the transfer of normal microbiota from wild-type mice. Mechanistically, DOK3 exerts its protective effect by suppressing JAK2/STAT3 signaling in colonic neutrophils to limit their S100a8/9 production, thereby maintaining gut microbial ecology and colon homeostasis. Hence, our findings reveal that the immune system and microbiome function in a feed-forward manner, whereby DOK3 maintains colonic neutrophils in a quiescent state to establish a gut microbiome essential for intestinal homeostasis and protection from IBD.
2021-11-10 | GSE186597 | GEO
Project description:This project used glycomics approach to study the N-glycan present at the intestinal mucosal-luminal interface of pediatric UC patients.
2022-03-01 | PXD026327 | Pride
Project description:BACKGROUND & AIMS: Toll-like receptor 2 (Tlr2) is important in bacterial pattern recognition and has been recognized as a modifier of intestinal inflammation. In this study we sought to determine the epigenomic, transcriptomic and microbiomic consequences of Tlr2 deficiency in the colonic mucosa of mice to gain insights into biological pathways that shape the interface between the gut microflora and the mammalian host. METHODS: Colonic mucosa from C57BL/6 and Tlr2-/- mice was interrogated by methylation specific amplification microarray (MSAM) to screen for changes in DNA methylation, with bisulfite pyrosequencing validation. Transcriptomic changes in the same tissue were analyzed by microarray expression profiling and real time RT-PCR. The mucosal microbiome was studied by high throughput, detailed pyrosequencing of 16S RNA. RESULTS: Tlr2 deficiency influenced the methylation of about 1% of the interrogated genome and resulted in a significant expression change in a similar percentage of all transcripts studied. Importantly, gene ontology analysis revealed that the expression of genes involved in immune processes is significantly modified by the absence of Tlr2, some of which have been already linked to inflammatory bowel diseases (Stat1, Anpep), for example. Overlaps between DNA methylation and gene expression changes were confirmed at Anpep and Ifit2. The epigenomic and transcriptomic modifications associated with alteration in mucosal microbial composition, affecting 11% of the detected bacterial species in the Tlr2-/- animals. CONCLUSIONS: Tlr2 deficiency induces colonic mucosal epigenomic, transcriptomic and microbiomic changes underscoring the intricate network of biological processes that provide the link between genotype and phenotype in mammals. Our findings bare implications for common gastrointestinal disorders such as IBD and colon cancer.
2010-07-01 | GSE21845 | GEO