Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA281486 | ENA |
REPOSITORIES: ENA
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| PRJNA290867 | ENA
Project description:To further development of our gene expression approach to CD300a deficiency on dendritic cells (DCs) in colonic lamina propria, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish CD300a deficiency on DCs in colonic lamina propria from those of WT mice. Colonic lamina propria DCs were obtained by cell sorter from WT and CD300a deficient mice raised under SPF and GF condition. Expression of Ifnb1 was significantly higher in CD300a deficient DCs, quantified in the same RNA samples by real-time PCR. Gene expression in WT and CD300a colonic lamina propria DCs raised under SPF and GF conditions were measured. Colonic lamina propria cells were obtained from 5 mice in each conditions. Takara-Bio
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Project description:The IL-33 receptor ST2 is differentially expressed by colonic lamina propria Treg cells Microarray of sort-purified Foxp3+ Treg cells from colonic lamina propria over mesenteric lymph node
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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
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BIOMD0000000583.
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2014-04-08 | BIOMD0000000583 | BioModels
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2015-07-25 | E-GEOD-68009 | biostudies-arrayexpress
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2013-04-09 | E-GEOD-45881 | biostudies-arrayexpress
Project description:To further development of our gene expression approach to CD300a deficiency on dendritic cells (DCs) in colonic lamina propria, we have employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential to distinguish CD300a deficiency on DCs in colonic lamina propria from those of WT mice. Colonic lamina propria DCs were obtained by cell sorter from WT and CD300a deficient mice raised under SPF and GF condition. Expression of Ifnb1 was significantly higher in CD300a deficient DCs, quantified in the same RNA samples by real-time PCR.
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