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Expression data from study on IL33 signaling in Dusp5 deficient eosinophils

ABSTRACT: Dusp5 regulates ERK phosporylation following IL-33 receptor ligation in cultured eosinophils. Dusp5 deficient eosinophils show increased ERK phosphorylation, and as a result are less apoptotic. Since ERK stimulation results in downstream activation of transcription factors, we are utilizing a microarray approach to find alterations in gene expression to uncover potential mechanisms for increased cell survival. Day 12 bone marrow derived eosinophils from Dusp5+/+ and Dusp5-/- mice (5 mice per genotype) were left untreated (media only) or IL-33 (25ng/ml) stimulated for 4 hours. Treated cells were washed with ice cold PBS and cell pellets were directly lysed in RLT buffer (Qiagen) followed by immediate RNA isolation (RNEasy plus mini kit with genomic DNA eliminator columns). Sample group names: Group 1- Dusp5+/+ Untreated (N=5) Group 2- Dusp5-/- Untreated (N=5) Group 3- Dusp5+/+ IL-33 4hrs (N=5) Group 4- Dusp5-/- IL-33 4hrs (N=5) Sample Names: Group 1- BM Eos unstimulated WT-1....WT-5 Group 2- BM Eos unstimulated Dusp5-/- -1......Dusp5-/- -5 Group 3- BM Eos IL-33 4hrs WT-1....WT-5 Group 4- BM Eos IL-33 4hrs Dusp5-/- -1......Dusp5-/- -5

ORGANISM(S): Mus musculus

SUBMITTER: Derek Holmes

PROVIDER: E-GEOD-62999 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from study on IL33 signaling in Dusp5 deficient eosinophils

Project description:Dusp5 regulates ERK phosporylation following IL-33 receptor ligation in cultured eosinophils. Dusp5 deficient eosinophils show increased ERK phosphorylation, and as a result are less apoptotic. Since ERK stimulation results in downstream activation of transcription factors, we are utilizing a microarray approach to find alterations in gene expression to uncover potential mechanisms for increased cell survival.

2014-11-06 | GSE62999 | GEO

IL-33 markedly induces murine eosinophil gene transcription via autocrine IL-4-dependent and -independent mechanisms

Project description:Eosinophils are major effector cells in type 2 inflammatory responses and become activated in response to IL-4 and IL-33, yet the molecular mechanism remains unclear. We examined the direct effect of these cytokines on eosinophils and demonstrated that murine eosinophils respond to IL-4 and IL-33 by phosphorylation of STAT-6 and NFkB, respectively. RNA sequencing analysis of murine eosinophils indicated that IL-33 regulates 519 genes, whereas IL-4 regulates only 28 genes, including 19 IL-33-regulated genes. Interestingly, IL-33 induced eosinophil activation via two distinct mechanisms, IL-4 independent and IL-4 secretion/auto-stimulation dependent. Anti-IL-4 or anti-IL-4Ra antibody-treated eosinophils, as well as Il4- or Stat6-deficient eosinophils, had attenuated protein secretion of a subset of IL-33-induced genes, including Retnla and Ccl17. However, the induction of most IL-33-regulated transcripts (e.g. Il6 and Il13) was IL-4 independent and blocked by NFkB inhibition. Indeed, IL-33 induced the rapid release of pre-formed IL-4 protein from eosinophils by an NFkB-dependent mechanism. Thus, we have identified a novel activation pathway in murine eosinophils that is induced by IL-33 and differentially dependent upon IL-4. These data suggest that IL-4 plays a critical role in auto-amplification of IL-33-induced eosinophil activation and could be a potential target for therapeutic approaches in IL-33-related eosinophil-associated diseases. Low density bone marrow derived murine eosinophils were generated in culture over the period of 14 days. Eosinophils were activated by either IL-33 or IL-4 at 10 ng/ml for 1hr and 4hr. RNA was collected and subjected to next generation sequencing.

2013-08-01 | E-GEOD-43660 | biostudies-arrayexpress

Transcriptomic response to ex vivo IL33 stimulation of blood eosinophils from mepolizumab- or omalizumab-treated patients

Project description:Coding RNA expression of blood eosinophils from mepolizumab- or omalizumab-treated patients stimulated ex vivo with IL-33 for 6 hours and of directly processed non-stimulated blood eosinophils from the same samples (paired design)

2021-12-17 | E-MTAB-10189 | biostudies-arrayexpress

Comparison of coding RNA expression in steady-state and in response to IL33 and IL5 stimulation in bone marrow eosinophils from IL5-deficient and wild-type littermates

Project description:Aim of the experiment was to assess differences in expression of coding RNA between bone marrow eosinophils arising in IL-5 knock-out mice (C57BL/6-Il5tm1Kopf/J) or wild-type littermates and their response to cytokine stimulation. Bone marrow eosinophils were sorted by FACS submitted to RNA-seq immediately or after 4 hours of stimulation with IL-5 and IL-33 in culture plates.

2021-12-17 | E-MTAB-10188 | biostudies-arrayexpress

IL-33 markedly induces murine eosinophil gene transcription via autocrine IL-4-dependent and -independent mechanisms

2013-08-01 | GSE43660 | GEO

Segmental Allergen Challenge Regulates Gene Expression In Bronchoalveolar Lavage (BAL) Cells From Atopic and Mild Asthmatic Subjects

Project description:Segmental allergen challenge increases the percentage of eosinophils in bronchoalveolar lavage (BAL) cells. Mepolizumab, an anti-IL-5 therapeutic antibody, decreases the number of eosinophils in bronchoalveolar lavages (BAL). The use of both procedures allows to define genes that are either expressed by eosinophils or dependent on eosinophil presence in the airways. Cells from Bronchoalveolar lavages (BAL) are obtained by bronchoscopy before (V5) and 48 h after a segmental allergen challenge (V6) in atopic and mild astmatics. This procedure was repeated in the same two subjects 2 months later and 1 month after an injection of mepolizumab (V22 is before challenge and V23 after challenge). Cells were immediately lysed and isolated total RNAs were analyzed using the Human Genome 1.0 ST GeneChip arrays (Affymetrix, Santa Clara, CA).

2013-05-01 | E-GEOD-46159 | biostudies-arrayexpress

Characterization of long-term IL-33 administration as an animal model of pulmonary arterial hypertension

Project description:Pulmonary arterial hypertension (PAH) is characterized by severe obstruction of small pulmonary arteries and concomitant high pulmonary arterial pressure, resulting in progressive right ventricular failure. Previously, we demonstrated that long-term interleukin (IL)-33 administration in mice induced severe occlusive arterial hypertrophy in the lung, which was mediated by group 2 innate lymphoid cells (ILC2s). In response to IL-33, ILC2s accumulated around blood vessels and produced IL-5, leading to perivascular eosinophil recruitment. In this study, we further characterized IL-33-induced pulmonary arterial hypertrophy. We first demonstrated that long-term IL-33 administration caused an increase in the right ventricular pressure. In IL-33 deficient mice, pulmonary arterial hypertrophy mediated by eggs of Schistosoma mansoni (S. mansoni) was attenuated, accompanied with partial reduction in ILC2s, eosinophils and CD4+ T cells. In addition, proteomic analysis revealed dramatic changes in urine samples from mice treated with IL-33 or S. mansoni eggs. Resistin like alpha (RELM), a pulmonary hypertension-related molecule, in the urine was commonly detected in both treatments. Large amounts of RELM were observed in the lung from IL-33-treated mice. These observations support that IL-33-induced pulmonary arterial hypertrophy is a useful model to study the mechanism underlying development of PAH and expolar biomarkers to indicate the onset of PAH.

2024-09-27 | PXD055773 | JPOST Repository

Time-course Activation of Human Peripheral Blood Eosinophils by Cytokines

Project description:Activated eosinophils contribute to airway dysfunction and tissue remodeling in asthma, and thus are considered an important factor in asthma pathology. We report here comparative proteomic and phosphoproteomic changes upon activation of eosinophils using eight cytokines individually and in selected cytokine combinations, in time-course reactions. Differential protein and phosphoprotein expressions were determined by mass spectrometry after 2-dimensional gel electrophoresis (2DGE) followed by protein identification by MS, and by label-free LC-MS/MS. We found that each cytokine-stimulation produced significantly different changes in the eosinophil proteome and phosphoproteome, with phosphoproteomic changes being more pronounced and having an earlier onset. Furthermore, we observed that IL-5, GM-CSF, and IL 3 showed the greatest change in protein expression and phosphorylation, and this expression differed markedly from those of the other five cytokines evaluated. Comprehensive univariate and multivariate statistical analyses were employed to evaluate the comparative results. We also monitored eosinophil activation using flow cytometry (FC) analysis of CD69 expression. In agreement with our proteomic studies, FC indicated that IL-5, GM-CSF, and IL-3 were more effective than the other five cytokines studied in stimulating a cell surface CD69 increase indicative of eosinophil activation. Moreover, selected combinations of cytokines revealed proteomic patterns with many proteins in common with single cytokine expression patterns but also showed a greater than additive effect of the two cytokines employed, indicating a more complex signaling pathway that was reflective of a more typical inflammatory pathology.

2017-12-19 | PXD004043 | Pride

Eosinophils scRNA-seq from healthy and asthmatic donors

Project description:scRNA-seq data from human eosinophils purified from blood samples. Samples include three healthy patients and three asthmatic donors.

2024-04-23 | E-MTAB-14010 | biostudies-arrayexpress

Interleukin-33 contributes to anemia of chronic inflammation by inhibiting differentiation of erythroid progenitors

Project description:Mature blood cells are produced continuously from hematopoietic stem and progenitor cells (HSPCs) in the bone marrow (BM). During chronic inflammation, this process may be perturbed by inflammatory cytokines acting on HSPCs to cause anemia of inflammatory disease. Among BM HSPCs, we found the receptor for interleukin (IL)-33, ST2, was expressed preferentially and highly on erythroid progenitors. Induction of inflammatory spondyloarthritis in mice increased IL-33 in BM plasma, and IL-33 was required for inflammation-dependent suppression of erythropoiesis in BM. Conversely, administration of IL-33 in healthy mice suppressed erythropoiesis, decreased hemoglobin expression, and caused anemia. Using purified erythroid progenitors in vitro, we showed that IL-33 directly inhibited terminal maturation. This effect was dependent on NF-kB activation and was associated with altered signalling events downstream of the erythropoietin receptor. Accordingly, IL-33 also suppressed erythropoietin-induced stress erythropoiesis in vivo. These results reveal a role for IL-33 in regulation of erythropoiesis during inflammatory disease and define a new target for its treatment.

2020-05-15 | GSE141480 | GEO

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