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IL-22+ T cells protect intestinal crypts from bacterial invasion and epithelial damage.

ABSTRACT: IL-22+ T cells protect intestinal crypts from bacterial invasion and epithelial damage.

PROVIDER: PRJNA471022 | ENA |

REPOSITORIES: ENA

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IL-22+ T cells protect intestinal crypts from bacterial invasion and epithelial damage.

Project description:Three subsets of intestinal epithelial cells (IECs) (P9, Surface; P10, Large Crypt; P11, Small Crypt) were isolated from Naïve and Day 9 C.r.-infected Cntrl (Cre-) and CD4 cre+. Il22 floxed mice (CD4 cKO)

2023-05-30 | GSE114338 | GEO

Gene expression data from DSS-treated crypts, normal colon crypts and tumor crypts

Project description:Comparative gene expression profiling between DSS-treated crypts and normal colon crypts Comparative gene expression profiling between normal colon crypts and tumor crypts

2017-01-01 | GSE56050 | GEO

Multiple DNA repair pathways collectively protect against DNA damage-induced replicative aging.

Project description:We demonstrate that transcriptomic profiling of the NER mutant ercc-1 offers better understanding of the complex phenotypes of ercc-1 deficiency in C. elegans, as it does in mammalian models. There is a transcriptomic shift in ercc-1 mutants that suggests a stochastic impairment of growth and development, with a shift towards a higher proportion of males in the population. Extensive phenotypic analyses confirm that NER deficiency in C. elegans leads to severe developmental and growth defects and a reduced replicative lifespan, although post-mitotic lifespan is not affected. Results suggest that these defects are caused by an inability to cope with randomly occurring DNA damage, which may interfere with transcription and replication. The study investigates the developmental and aging phenotypes of different NER deficient C. elegans mutants (xpa-1, ercc-1, xpf-1 and xpg-1), where the transcriptomic profile of ercc-1 mutant is presented. We show that loss of NER function does not affect post-mitotic lifespan, but leads to impaired embryogenesis, germ cell and larval development and causes a reduced replicative lifespan. Phenotypes are most pronounced in ercc-1, xpf-1 and xpg-1 mutant animals. We provide evidence that this more pronounced phenotype is likely caused by the fact that these genes are involved in multiple repair pathways besides NER. Furthermore, transcriptional profiling of ercc-1 mutants confirms these observations, showing that growth and developmental pathways are underrepresented but that insulin signaling is not affected. Our analysis suggests that XPA-1, ERCC-1, XPF-1 and XPG-1 protect animals against replicative aging by preventing the accumulation of randomly acquired DNA damage. Eight mixed stage C. elegans samples were run on Affymetrix GeneChip C. elegans Genome Arrays. Four samples belong to ercc-1 mutant group and four to the wild-type, N2.

2013-09-15 | E-GEOD-39145 | biostudies-arrayexpress

THC Protect

Project description:Thc protect llc

| PRJNA1097369 | ENA

IL-22 promotes postnatal formation of MUC17 glycocalyx barrier that protects host enterocytes

Project description:The apical aspects of absorptive epithelial cells form a highly organized brush border membrane (BBM), shaped by densely packed microvilli that are coated with a glycocalyx. Here, we present evidence showing that the glycocalyx forms an epithelial barrier that prevents exogenous molecules from gaining access to the BBM. We used a multiomics approach to investigate function and regulation of membrane mucins exposed on the enterocytic BBM during postnatal development of the small intestine. Muc17 was identified as a major membrane mucinin the glycocalyx that was specifically upregulated by IL-22 as part of an epithelial defense repertoire during suckling-weaning transition. High levels of IL-22 at the time of weaning primed progenitor enterocyte to express Muc17 as they migrate out of intestinal crypts to replace neonatal enterocytes. Our findings propose a role for membrane mucin Muc17 in epithelial barrier function in the small intestine.

2021-02-16 | PXD018592 | Pride

Interleukin-22 immunotherapy modulates pulmonary gene expression evocative of enhanced tissue barrier and reduces bacterial systemic invasion during severe influenza

Project description:Severe bacterial (pneumococcal) infections are commonly associated with influenza and are significant contributors to the excess morbidity and mortality of influenza. Disruption of lung tissue integrity during influenza participates in bacterial pulmonary colonization and dissemination out of the lungs. Interleukin (IL)-22 has gained considerable interest in anti-inflammatory and anti-infection immunotherapy over the last decade. In the current study, we investigated the effect of exogenous IL-22 delivery on the outcome of bacterial superinfection post-influenza. Our data show that exogenous treatment of influenza-infected mice with recombinant IL-22 reduces bacterial dissemination out of the lungs but is without effect on pulmonary bacterial burden. We describe an IL-22 specific gene signature in the lung tissue of IAV-infected (and naÃ¯ve) mice that might explain the observed effects. Indeed, exogenous IL-22 modulates gene expression profile in a way suggesting a reinforcement of tissue integrity. Our results open the way to alternative approaches for limiting post-influenza bacterial superinfection, particularly systemic bacterial invasion.

2018-05-31 | E-MTAB-6044 | biostudies-arrayexpress

Gene expression profiling of genes differentially expressed by oral carcinoma Ca9-22 and SLPI-deficient Ca9-22 (ΔSLPI) cells

2016-08-22 | GSE78501 | GEO

Metabolic enzymes moonlight as selective autophagy receptors to protect plants against viral induced cellular damage

Project description:Metabolic enzymes moonlight as selective autophagy receptors to protect plants against viral induced cellular damage

| PRJNA1103879 | ENA

Transcription profiling of human vascular smooth muscle cells treated with glucose oxidase and human haemoglogib reveals ferrous hemoglobin can protect vascular smooth muscle cells from hydrogen peroxide-induced oxidative stress response and cell damage

Project description:Hemoglobin (Hb) is released from red blood cells (RBC) during intravascular hemolysis. Cell free Hb has been implicated to play a pathogenic role in hemolytic diseases such as sickle cell anemia or malaria. Hydrogen peroxide (H2O2) is the most prevalent reactive oxygen species which is produced in excess during inflammation or tissue injury and has been included as a potential mediator of oxidative stress related cell and tissue damage. The biologic significance of Hbs peroxidase activity as an anti-oxidant is controversial as the radicals and higher oxidation iron species which are potentially released during these reactions could be a source of exaggerated oxidative damage. Using a cell culture model of low-flux continuous H2O2 generation by glucose-oxidase (GOx) Hb revealed the potential to protect vascular smooth muscle cells and macrophages from H2O2 mediated glutathione depletion and cell death. As revealed by gene array analysis, Hb effectively abolished H2O2 induced oxidative stress response in these cells. Through electron microscopy and quantitative mass spectrometry extensive oxidation of specific Hb amino acid residues, polymerization and precipitation was defined. This may be a consequence of potential protective mechanism within Hb. The net biologic effect of Hb, when present in oxidative rich environments, is likely a result of the balance of H2O2 consumption (protection) on one hand and the production of free radicals (damage) on the other hand. Further the extensive structural changes occurring during the reaction of ferrous Hb with H2O2 could 'absorb' a significant amount of oxidative impact and thereby further protect the environment from heme derived free radical damage. The intrinsic peroxidase activity of hemoglobin seems to be a constitutive 'enzymatic' function of Hb which adds a novel facet to the multivalent role played by the abundant oxygen carrier protein.

2009-09-15 | E-MEXP-2263 | biostudies-arrayexpress

Gene expression profiling of genes differentially expressed by oral carcinoma Ca9-22 and SLPI-deficient Ca9-22 (ÎSLPI) cells

Project description:We used the myoma model in conjunction with gene expression profiling with microarray data as an efficient tool for high throughput analysis and to screen for differentially expressed genes. Our aim was to identify candidates playing an important role in SLPI and/or MMP-promoted tumor invasion by comparing oral carcinoma Ca9-22 cells, which highly express secretory leukocyte protease inhibitor (SLPI) gene, with SLPI-deficient Ca9-22 cells. In oral carcinoma Ca9-22 and SLPI-deficient Ca9-22 (ÎSLPI) samples, gene expression profiling was performed with the Affymetrix Human Genome U133 Plus 2.0 Array. Two arrays for 2 cell lines were analyzed.

2016-08-22 | E-GEOD-78501 | biostudies-arrayexpress

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