Gene expression profiles in the ileal and colonic epithelial cells from Interleukin (IL)-23-deficient mice and IL-22-deficient mice
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PROVIDER: PRJNA990813 | ENA |
REPOSITORIES: ENA
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Project description:To investigate the function of IL-23 and IL-22 on the intestinal epithelial cells, we analyzed the gene expression profiles in ileal and colonic epithelial cells of mice deficient in IL-23 and IL-22.
2023-09-08 | GSE236445 | GEO
Project description:IL-13 plays a key role during protective type 2 immune responses at mucosal sites, such as during infection with nematodes. However, dysregulation of IL-13 can also contribute to the pathogenesis of allergic and fibrotic diseases. Matrix remodelling is an important component of repair processes in the lung but is also a hallmark of chronic diseases such as asthma. Since IL-13 shares receptors and signalling pathways with IL-4, disentangling the relative contributions of these two type 2 cytokines has been challenging. Additionally, little is known about the singular role of IL-13 in more acute settings of tissue injury/repair and whether IL-13 regulates remodelling of the extracellular matrix following tissue injury. In this study, we used Nippostrongylus brasiliensis infection as model of acute lung tissue damage and repair by comparing responses between WT and IL-13-deficient mice, in which IL-4 signalling is intact.
2021-06-11 | PXD021853 | Pride
Project description:The Th2 cytokine IL-13 has been described to be involved in biliary epithelial injury and liver fibrosis in patients as well as in animal models. IL-13 was found to reduce tight junction-associated barrier function of bile ducts, to promote cholangiocyte hyperplasia, and thus causing biliary epithelial injury. We generated Abcb4-/-- and IL-13-/- double-knockout mice on fibrosis susceptible genetic background BALB/c. Molecular and cellular mechanisms of hepatic and ileal pathology were investigated by mRNA microarray. Depletion of IL-13 in Abcb4-/--mice resulted in a tenfold decrease of total serum bile acid concentrations at the age of 8 weeks and lead to a recovery of intrahepatic bile duct integrity. The decrease of serum bile acid in 8 week old mice went along with relative enhancement of bile acid excretion and normalization of the composition of fecal bile excretion, correction of fecal microbiome, and improved ileal integrity. Liver integrity, measured by serum ALT, was ameliorated in younger mice and strongly correlated with the concentration of serum bile acids. 52 weeks old Abcb4-/-IL-13-/--mice exhibited significantly reduced hepatic fibrosis.
2020-11-02 | GSE90995 | GEO
Project description:Background and aimsThe impairment of intestinal epithelial barrier is the main etiologic factor of inflammatory bowel disease. The proper intestinal epithelial proliferation and differentiation is crucial for maintaining intestinal integrity. Metformin is a common anti-diabetic drug. The objective is to evaluate the protective effects of metformin on ileal epithelial barrier integrity using interleukin-10 deficient (IL10KO) mice.MethodsWild-type and IL10KO mice were fed with/without metformin for 6 weeks and then ileum was collected for analyses. The mediatory role of AMP-activated protein kinase (AMPK) was further examined by gain and loss of function study in vitro.ResultsCompared to wild-type mice, IL10KO mice had increased proliferation, reduced goblet cell and Paneth cell lineage differentiation in the ileum tissue, which was accompanied with increased crypt expansion. Metformin supplementation mitigated intestinal cell proliferation, restored villus/crypt ratio, increased goblet cell and Paneth cell differentiation and improved barrier function. In addition, metformin supplementation in IL10KO mice suppressed macrophage pro-inflammatory activity as indicated by reduced M1 macrophage abundance and decreased pro-inflammatory cytokine IL-1?, TNF-? and IFN-? expressions. As a target of metformin, AMPK phosphorylation was enhanced in mice treated with metformin, regardless of mouse genotypes. In correlation, the mRNA level of differentiation regulator including bmp4, bmpr2 and math1 were also increased in IL10KO mice supplemented with metformin, which likely explains the enhanced epithelial differentiation in IL10KO mice with metformin. Consistently, in Caco-2 cells, metformin promoted claudin-3 and E-cadherin assembly and mitigated TNF-?-induced fragmentation of tight junction proteins. Gain and loss of function assay also demonstrated AMPK was correlated with epithelial differentiation and proliferation.ConclusionsMetformin supplementation promotes secretory cell lineage differentiation, suppresses inflammation and improves epithelial barrier function in IL10KO mice likely through activation of AMPK, showing its beneficial effects on gut epithelial.
| S-EPMC5176295 | biostudies-literature
Project description:To further understand immune mechanims involved in regulating intestinal inflammation, we employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential of regulating inflammation in the absence of IL-10. Whole colon tissue from IL-10-deficient and C57BL/6 (wild-type) mice was collected 2 weeks after Citrobacter rodentium infection and from uninfected controls. Consistent with the histological and cellular analysis, expression levels of many chemokines and cytokines involved in recruiting leukocytes and promoting inflammation were, on average, lower in IL-10 deficient compared to wild-type mice after infection. An exception to this general trend was IL-27, a cytokine with both pro- and anti-inflammatory properties. Two weeks after Citrobacter rodentium challenge, total RNA was extracted and analyzed from whole colon tissue of infected IL-10-deficient and wild-type mice, and compared to uninfected controls. Each sample contained equal amounts of total RNA from 4-5 female mice which were pooled and used in the experiment.
2014-03-12 | E-GEOD-55812 | biostudies-arrayexpress
Project description:To elucidate IL-17A-dependent immune mechanims involved in regulating host defense, we employed whole genome microarray expression profiling as a discovery platform to identify genes with the potential of regulating protective immunity that failed to be upregulated in the absence of IL-17RA signaling. Whole small intestine tissue collected from IL-17RA-deficient and C57BL/6 (wild-type) mice was collected 2 weeks after Giardia muris infection and from uninfected controls. Expression levels of several genes that may have anti-parasitic potential (Defb1, Retnlb, Saa1, Saa2) and may be involved in parasite clearance were, on average, lower or unchanged in IL-17RA deficient compared to wild-type mice after infection. Two weeks after Giardia muris challenge, total RNA was extracted and analyzed from tissue of the small intestines of infected IL-17RA-deficient and wild-type mice, and compared to uninfected controls. Each sample contained equal amounts of total RNA from 6 female mice which were pooled and used in the experiment.
2015-05-15 | E-GEOD-68868 | biostudies-arrayexpress
Project description:BackgroundThe concept that a strong inflammatory response involving the full complement of cytokines and other mediators is critical for unimpaired healing has been challenged by wound healing studies using transgenic and knockout (KO) mice. The present study explored the effect of abrogation of the p40 subunit, which is shared by the pro-inflammatory cytokines interleukin (IL)-12 and IL-23, on wound closure of excisional oral mucosal wounds.MethodsDouble IL-12 and IL-23 KO mice and C57BL ? 6J wildtype mice were wounded on the dorsal surface of the tongue using a 2 mm biopsy punch. The degree of epithelialization was examined histologically. At specific timepoints wounds were examined for cellular and molecular markers for inflammation and angiogenesis using 1) immunohistochemistry; 2) analysis of RNA expression; and 3) flow cytometric analysis.ResultsCompared to wild type controls, KO mice displayed enhanced healing, which was driven by a greater influx of neutrophils and macrophages during the early stages of wound healing, and increased induction of messenger RNA (mRNA) for endothelial derived neutrophil attractant (ENA78) chemokine and macrophage inflammatory protein-2 alpha (MIP-2?). Increased mRNA for monocyte-attracting chemokines including monocyte chemoattractant protein (MCP)-1 and MCP-3 was seen from day 1, together with higher levels of IL-1? and IL-6 within 24 hours after wounding. In addition, mRNA for vascular endothelial growth factor (VEGF)-A was upregulated in KO mice within 2 hours after injury, and higher expression of this mediator was confirmed by immunohistochemistry.ConclusionOverall, the accelerated oral mucosal wound healing seen in IL-12/IL-23p40 KO compared to wildtype mice was associated with the early establishment of an inflammatory response and vascularization.
| S-EPMC3296624 | biostudies-literature
Project description:To define the IL-23R-dependent changes in intestinal regulatory T cells (Treg cells) that might contribute to the impact on Treg cell function and selective advantage
2023-02-17 | GSE208621 | GEO
Project description:Bulk RNA-seq of interleukin-23 receptor (IL-23R) -deficient and IL-23R-sufficient colonic mouse regulatory T cells
| PRJNA860355 | ENA
Project description:Previous studies of our group have shown that IL-25 is essential for the resistance to E. caproni infections and the susceptibility of mice relies on the inability of this host species to produce IL-25 in response to infection (14-15). Susceptibility of mice to primary E. caproni infection was associated with low levels of intestinal IL-25 expression, whilst deworming via administration of praziquantel (pzq) was accompanied by a steady increase in IL-25 expression and, in turn, by the onset of a Th2-type response that prevented the establishment of secondary infections (14-15). Although these facts, little is known about the mechanism by which IL-25 generates resistance against intestinal helminths. In the present work, we analyze the changes in the production of proteins induced by IL-25 in the ileum of mice that may be involved in the generation of resistance against intestinal helminths.
2021-09-09 | PXD019477 | Pride