Expression data from pulmonary Type 2 Myeloid (T2M) cells, Eosinophils, Neutrophils, and Macrophages, from IL-25 treated 4get mice
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE36392 | GEO | 2012/03/10
SECONDARY ACCESSION(S): PRJNA153281
REPOSITORIES: GEO
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Project description:Many symptoms associated with allergic asthma result from the sequelae of type 2 inflammation. Interleukin (IL)-25 promotes type 2 inflammatory responses, and T2M cells represent an IL-4 and IL-13 producing granulocytic IL-25 responsive population. We used microarrays to characterize the gene expression profile of T2M cells, and compared T2M cells to other inflammatory subsets (eosinophils, neutrophils, and macrophages) in the lungs of mice with IL-25-induced pulmonary inflammation. Inflammatory subsets were isolated from the lungs of IL-25 treated 4get mice for RNA extraction and hybridization on Affymetrix microarrays. We pooled cells from 4 donor mice for each replicate, and used FACS to isolate pure populations of each inflammatory subset in parallel. We analyzed 3 T2M replicates and 2 replicates each of the other inflammatory subsets.
2012-03-10 | E-GEOD-36392 | biostudies-arrayexpress
Project description:Triggering Receptor Expressed on Myeloid cells 1 (TREM-1) an innate receptor that canonically amplifies inflammatory signaling in neutrophils and monocytes, plays a central role in regulating lung inflammation. Utilizing a murine model of asthma, flow cytometry revealed TREM-1+ eosinophils in the lung tissue and airway during allergic airway inflammation. TREM-1 expression was restricted to recruited, inflammatory eosinophils. Expression was induced on bone marrow derived eosinophils by incubation with IL-33, LPS, or GM-CSF. Compared to TREM-1- airway eosinophils, TREM-1+ eosinophils were enriched for pro-inflammatory gene sets including migration, respiratory burst, and cytokine production. Unexpectedly, eosinophil-specific ablation of TREM-1 increased airway IL-5 and lung tissue eosinophil accumulation. Further investigation of transcriptional data revealed apoptosis related gene sets were enriched in TREM-1+ eosinophils. Annexin V staining demonstrated higher rates of apoptosis among TREM-1+ eosinophils compared to TREM-1- eosinophils in the inflammatory airway. In vitro, Trem1/3-/- eosinophils were protected from apoptosis. Finally, inhibition of reactive oxygen species production with diphenyleneiodonium protected WT bone marrow derived eosinophils from apoptosis more than Trem1/3-/- eosinophils, suggesting that superoxide accounted for more apoptosis in WT cells. These data demonstrate protein level expression of TREM-1 by eosinophils for the first time, define a population of TREM-1+ inflammatory eosinophils, and reveal that eosinophil TREM-1 restricts key features of type 2 lung inflammation.
2023-12-15 | GSE246389 | GEO
Project description:Memory helper T cells provide long-lasting host defeMemory helper T cells provide long-lasting host defense against microbial pathogens, while distinct subpopulations of memory T cells drive chronic inflammatory diseases such as asthma. Asthma is a chronic allergic inflammatory disease with airway remodeling including fibrotic changes. The immunological mechanisms that induce airway fibrotic changes in allergic inflammation remain unknown. We found that Interleukin-33 (IL-33) enhanced Amphiregulin production by the IL-33 receptor, ST2hi memory T helper-2 (Th2) cells. Amphiregulin-epidermal growth factor receptor (EGFR)-mediated signaling directly reprogramed eosinophils to an inflammatory state with enhanced production of Osteopontin, a key profibrotic immunomodulatory protein. IL-5-producing memory Th2 cells and Amphiregulin-producing memory Th2 cells appeared to cooperate to establish lung fibrosis. The analysis of polyps from patients with eosinophilic chronic rhinosinusitis revealed fibrosis with accumulation of Amphiregulin-producing CRTH2hiCD161hiCD45RO+CD4+ Th2 cells and Osteopontin-producing eosinophils. Thus, the IL-33-Amphiregulin-Osteopontin axis directs fibrotic responses in eosinophilic airway inflammation and is a potential target for the treatment of fibrosis induced by chronic allergic disorders. against microbial pathogens, while distinct subpopulations of memory T cells drive chronic inflammatory diseases such as asthma. Asthma is a chronic allergic inflammatory disease with airway remodeling including fibrotic changes. The immunological mechanisms that induce airway fibrotic changes in allergic inflammation remain unknown. We found that Interleukin-33 (IL-33) enhanced Amphiregulin production by the IL-33 receptor, ST2 hi memory T helper-2 (Th2) cells. Amphiregulin-epidermal growth factor receptor (EGFR)-mediated signaling directly reprogramed eosinophils to an inflammatory state with enhanced production of Osteopontin, a key profibrotic immunomodulatory protein. IL-5-producing memory Th2 cells and Amphiregulin-producing memory Th2 cells appeared to cooperate to establish lung fibrosis. The analysis of polyps from patients with eosinophilic chronic rhinosinusitis revealed fibrosis with accumulation of Amphiregulin-producing CRTH2hiCD161hiCD45RO+CD4+ Th2 cells and Osteopontin-producing eosinophils. Thus, the IL-33-Amphiregulin-Osteopontin axis directs fibrotic responses in eosinophilic airway inflammation and is a potential target for the treatment of fibrosis induced by chronic allergic disorders.
2018-08-21 | GSE114921 | GEO
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
Project description:The role of eosinophilic inflammation in chronic obstructive pulmonary disease (COPD) pathogenesis is unknown and is probably different than in asthma. The molecular processes underlying the differences between eosinophils from asthma and COPD have not been studied. The study group included 5 patients with asthma and 4 patients with COPD. The RNA-Seq data analysis identified 26 differentially expressed genes between COPD and asthma (according to adjusted p-value). In total, 6 genes were up-regulated (CCL3L1, CCL4L2, SERPINB2, PRSS21, GPR82) and 20 were down-regulated (e.g. JUN, IFITM3, DUSP1, GNG7, ZNF107, BCL6) in peripheral eosinophils of COPD patients compared to asthma. Biological processes associated with down-regulated genes were cell differentiation, positive regulation of RNA metabolic process. The genes associated with signaling of IL-4 and IL-13 pathway were down-regulated in COPD eosinophils compared to asthma. Peripheral eosinophils from COPD and asthma patients present different transcriptomic profiles suggesting their different function in pathobiology of both obstructive airway diseases.
2024-01-01 | GSE237284 | GEO
Project description:Purpose: we aimed to characterized eosinophils in the murine model of asthma Methods: Eosinophils were sorted from the lung of naïve and and HDM-induced asthma mice. There after RNA was extracted from the sorted eosinophils and subjected to RNAseq. Results:we demonstrated that resident lung eosinophils require IL-5 for their survival and that the expression of Siglec-F, is regulated by IL-5 . Conclusion: Our data suggest that the distinct eosinophil populations in the asthmatic lung represent a continuum of activation states rather than distinct eosinophil subsets.
2023-04-17 | GSE203225 | GEO
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. 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
2014-11-06 | E-GEOD-62999 | biostudies-arrayexpress
Project description:Aeroallergen sensing by airway epithelial cells can trigger pathogenic immune responses leading to chronic type 2 inflammation, the hallmark of airway diseases such as asthma. Airway tuft cells are specialized chemosensory epithelial cells and the dominant source of the epithelial cytokine IL-25 in the trachea and of cysteinyl leukotrienes (CysLTs) in the naïve murine nasal mucosa. How IL-25 and CysLTs might cooperatively promote type 2 inflammation in the airways has not been clarified. Here, we showed that inhalation of LTC4 in combination with a subthreshold dose of IL-25 led to dramatic synergistic induction of type 2 inflammation throughout the lungs, causing rapid eosinophilia, inflammatory type 2 innate lymphoid cell (ILC2) proliferation and type 2 cytokine production, dendritic cell (DC) and CD4+ T cell recruitment and goblet cell hyperplasia. While lung eosinophilia was dominantly mediated through the classical CysLT receptor CysLT1R, type 2 cytokines and activation of innate immune cells required signaling through both CysLT1R and CysLT2R. Tuft cell-specific deletion of Ltc4s, the terminal enzyme required for CysLT production, reduced lung inflammation and the systemic immune response after inhalation of the mold aeroallergen Alternaria; this effect was further enhanced by concomitant blockade of IL-25. Our findings identified a potent synergy of CysLTs and IL-25 downstream of aeroallergen-trigged activation of airway tuft cells leading to a highly polarized type 2 immune response and further implicate airway tuft cells as powerful modulators of type 2 immunity in the lungs.
2021-12-25 | GSE188820 | GEO
Project description:Dr. Paulson's group investigates the roles of carbohydrate-binding proteins involved in immune regulation and human disease, through their interaction with carbohydrate groups expressed on cell surface glycoconjugates. This laboratory is currently focused on how sialoside ligands modulate Siglec functions and on understanding the molecular basis of glycosylation changes following differentiation and activation of leukocytes. Three RNA preparations from IL-5 transgenic C567/B1 adult mouse eosinophils were sent to Microarray Core (E). The RNA was amplified, labeled, and hybridized to the GLYCOv3 microarrays. Data was analyzed to determine glycosyltransferase expression on mouse eosinophils, with specific interest in a cis-ligand of Siglec-F on eosinophils
2011-04-29 | E-GEOD-28923 | biostudies-arrayexpress
Project description:Eosinophilia is associated with various persisting inflammatory diseases and often coincides with chronic fungal infections or fungal allergy as in case of allergic bronchopulmonary aspergillosis (ABPA). However, the interactions between eosinophils and fungal pathogen leading to release of inflammatory mediators from eosinophils are poorly understood. Therefore, we established a co-culture system of mouse bone marrow derived eosinophils (BMDE) with Aspergillus fumigatus (Af) that we used in part to analyse transcriptional regulation induced by Af.
2022-05-31 | GSE165694 | GEO