Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1026559 | ENA |
REPOSITORIES: ENA
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Project description:Recent advances in (meta)genomic methods have provided new opportunities to examine host-microbe-environment interactions in the human gut. While opportunities exist to extract DNA from freshly sourced colonic tissue there are potentially valuable sources of DNA from historical studies that might also be examined. We examined how four different tissue DNA extraction methods employed in past clinical trials might impact the recovery of microbial DNA from a colonic tissue sample as assessed using a custom designed phylogenetic microarray for human gut bacteria and archaebacteria. While all methods of DNA extraction produced similar phylogenetic profiles some extraction specific biases were also observed. Real time PCR analysis targeting several bacterial groups substantiated this observation. These data suggest that while the efficacy of different DNA extraction methods differs somewhat all the methods tested produce an accurate representation of microbial diversity. This suggests that DNA samples archived in biobanks should be suitable for retrospective analyses. Three technical replicates per sample (extraction method) were analysed
2010-05-16 | E-GEOD-18420 | biostudies-arrayexpress
Project description:The gut microbiota plays a critical role in host energy metabolism and immune regulation, yet the temporal dynamics of microbial community responses to acute physiological stressors remain poorly characterized. While exercise is recognized as a modulator of gut microbial composition, the immediate post-exercise shifts in microbial community structure across different genetic backgrounds have not been systematically examined. Here, we present a longitudinal 16S rRNA gene sequencing dataset profiling the temporal dynamics of gut microbiota following acute high-intensity exercise in two widely used laboratory mouse strains. Age-matched male BALB/c and C57BL/6J mice were subjected to a single bout of acute exercise. The colonic content samples were collected to capture early temporal responsesat. Total genomic DNA was extracted from colonic contents and the 16S rRNA V4 region was amplified and sequenced on the NovaSeq6000 platform. This dataset enables identification of strain-specific and conserved exercise-responsive microbial taxa, and supports functional predictions related to energy metabolism and intestinal homeostasis.
2026-03-31 | GSE324758 | GEO
Project description:The oxidoreductases interleukin 4-induced gene 1 (IL4I1) and L-Amino acid oxidase 1 (LAO) are known to catalyze L-amino acid metabolism, yet their physiological roles in intestinal homeostasis remain largely unexplored. In this study, we investigated the impact of IL4I1 and LAO1 deficiency on colonic inflammation by generating wild-type, single knockout (IL4I1 KO and LAO1 KO), and double knockout (DKO) mice. Notably, DKO mice exhibited spontaneous diarrhea and histologically confirmed colitis, which were absent or rare in the other genotypes. Transcriptomic profiling and qRT-PCR analyses revealed upregulated expression of pro-inflammatory cytokines (IL-6, IL-17, IFN-γ) and Th1/Th17 transcription factors, along with overexpression of indoleamine 2,3-dioxygenase 1 (IDO1) in the colon of DKO mice. Metabolomic analysis indicated elevated colonic kynurenine levels and impaired metabolism of L-phenylalanine, L-tyrosine, and L-tryptophan. These changes were associated with a significant reduction in hydrogen peroxide (H₂O₂) production. Furthermore, 16S rRNA gene sequencing revealed altered beta diversity and reduced abundance of Short-chain fatty acid-producing bacteria in DKO mice. Among short-chain fatty acids, pentanoate was significantly decreased in DKO cecal contents. Collectively, these findings suggest that IL4I1 and LAO1 are essential for maintaining intestinal immune and metabolic balance. Their combined deficiency disrupts L-amino acid metabolism and H₂O₂-mediated regulation of the IDO1–kynurenine pathway, ultimately promoting gut dysbiosis and inflammatory diarrhea. This study provides novel insights into the metabolic and microbial mechanisms underlying colonic inflammation and highlights IL4I1 and LAO1 as potential targets for therapeutic intervention in inflammatory bowel diseases. This study provides novel insights into the metabolic and microbial mechanisms underlying colonic inflammation and highlights IL4I1 and LAO1 as potential targets for therapeutic intervention in inflammatory bowel diseases.
2026-06-28 | GSE300955 | GEO
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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2024-09-02 | BIOMD0000000583 | BioModels
Project description:Prostaglandins (PGs) are lipid signaling molecules that regulate diverse physiological and pathological processes, and their biosynthetic pathways are targets of widely used drugs such as aspirin and other nonsteroidal anti-inflammatory drugs (NSAIDs). However, previous research of PG biosynthesis has focused on host metabolic pathways, the roles of gut microbiota involved are not well understood 8. Here, we identify a colonic pathway through which gut microbes directly participate in PG metabolism and regulate colonic PG levels and their biological effects. Comparison of germ-free and conventionally raised mice reveals that the gut microbiota markedly increase the levels of multiple PGs in the colon. This effect is mediated by bacterial β-glucuronidases (GUS), which hydrolyze host-derived PG glucuronides, less active or inactive conjugates, to regenerate bioactive free PGs. GUS administration and bacterial mono-colonization in germ-free mice demonstrate a critical role for microbial GUS in regulating colonic PG levels and associated biological responses. Together, these findings reveal a previously unrecognized function of the gut microbiota in PG metabolism and identify microbial GUS enzymes as potential targets for modulating colonic PG signaling in gastrointestinal diseases.
2026-09-04 | GSE345950 | GEO
Project description:Microbial diversity of intestinal contents in mice
| PRJNA833531 | ENA