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Activated T cells secrete extracellular vesicles in the allergic airway that enhance eosinophil viability

ABSTRACT: Activated T cells secrete extracellular vesicles in the allergic airway that enhance eosinophil viability

PROVIDER: PRJNA1064163 | ENA |

REPOSITORIES: ENA

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Activated T cells secrete extracellular vesicles in the allergic airway that enhance eosinophil viability

Project description:T cells are not only central orchestrators of immune responses, but they drive tissue pathology in many inflammatory diseases. In allergic asthma, the activation of CD4+ T helper cells in response to allergens drives chronic type 2 lung inflammation characterized by the recruitment of eosinophils. Given the emerging roles of extracellular vesicles (EVs) as mediators of cell-to-cell communication, we hypothesized that T cells would secrete EVs in the lung to regulate the local inflammatory response. Using T cell specific membrane tagging and single vesicle flow cytometry, we found that T cell EVs are secreted into lung lining fluid during allergic inflammation in a mouse model of asthma. Functionally, EVs secreted by polarized T helper type 2 (Th2) cells promote eosinophil survival in vitro. This effect is only seen with EVs collected from Th2 cells activated through the T cell receptor. Activated Th2 cell EVs promote eosinophil survival by a surface-cargo dependent anti-apoptotic mechanism, inducing pro-survival and activation gene expression programs in these target cells. In vivo, activated Th2 cell EVs prolong eosinophilia in the lung after administration into the airways during allergic inflammation. Together, this study adds to emerging literature linking cellular activation state to EV function and supports a role for T cell EVs in enhancing tissue inflammation.

2025-07-03 | GSE253180 | GEO

Iron Drives Eosinophil Differentiation in Allergic Airway Inflammation through Mitochondrial Metabolic Adaptation

Project description:Understanding the metabolic mechanisms driving eosinophil differentiation in allergic airway inflammation is imperative for developing effective asthma therapies. Despite iron's well-established involvement in various cellular processes, its role in eosinophil differentiation remains elusive. This study observed elevated intracellular iron levels during eosinophil differentiation in the context of allergic airway inflammation. Through experiments involving iron-related compounds and specific diets, we demonstrated iron's indispensable role in promoting eosinophil differentiation, both in vitro and in vivo. Remarkably, an iron chelator effectively suppressed eosinophil differentiation and alleviated allergic airway inflammation. Mechanistically, iron maintains mitochondrial metabolic activities, mTORC1 signaling, and the expression of transcription factors that enforce eosinophil differentiation. Notably, iron influx rewires specific metabolic shifts in Krebs cycle, with succinate promoting eosinophil differentiation. Overall, this study highlights the significance of understanding the regulatory role of iron and underlying metabolic mechanisms in eosinophil differentiation, providing potential metabolic intervention strategies for asthma treatment.

2025-06-19 | GSE260684 | GEO

DJ-1 governs airway progenitor cell/eosinophil interactions to promote allergic inflammation

Project description:Background DJ-1 is an antioxidant protein known to regulate mast cell mediated allergic response, but its role in airway eosinophilic interactions and allergic inflammation is not known. Objective The aim of this study was to investigate the role of DJ-1 in airway eosinophilic inflammation in vitro and in vivo. Methods Ovalbumin-induced airway allergic inflammation was established in mice. ELISA was adopted to analyze DJ-1 and cytokine levels in mouse bronchoalveolar lavage fluid. Transcriptional profiling of mouse lung tissues was conducted by single-cell RNA sequencing technology. The role of DJ-1 in the differentiation of airway progenitor cells into goblet cells was examined by organoid cultures, immunofluorescence staining, quantitative PCR, and cell transplantation in normal, DJ-1 knockout (KO), or conditional DJ-1 KO mice. Results We observed that DJ-1 was increased in the lung tissues of ovalbumin-sensitized and challenged mice. DJ-1 KO mice exhibited reduced airway eosinophil infiltration and goblet cell differentiation. Mechanistically, we discovered that eosinophil-club cell interactions are reduced in the absence of DJ-1. Organoid cultures indicated that eosinophils impair the proliferative potential of club cells. Intratracheal transplantation of DJ-1-deficient eosinophils suppresses airway goblet cell differentiation. Loss of DJ-1 inhibits the metabolism of arachidonic acid into cysteinyl leukotrienes in eosinophils while these secreted metabolites promote airway goblet cell fate in organoid cultures and in vivo. Conclusion DJ-1-mediated interactions between airway epithelial progenitor cells and immune cells are essential in controlling airway goblet cell metaplasia and eosinophilia. Blockade of the DJ-1 pathway is protective against airway allergic inflammation.

2022-12-21 | GSE203079 | GEO

Mouse Eosinophil

Project description:MicroRNA have been implicated in the differentiation and control of eosinophilia in allergic inflammation, however, a detailed investigation of miRNA expression patterns employed during differentiation has not yet been performed [35-37]. The aim of our study is to explore miRNA expression profiling and analysis in silico in order to improve our understanding of the factors and circuits that are involved in the regulation eosinophil growth and differentiation.

2014-08-01 | E-MTAB-2442 | biostudies-arrayexpress

DJ-1 governs airway progenitor cell/eosinophil interactions to promote allergic inflammation

Project description:DJ-1 governs airway progenitor cell/eosinophil interactions to promote allergic inflammation

| PRJNA838489 | ENA

Iron Drives Eosinophil Differentiation in Allergic Airway Inflammation through Mitochondrial Metabolic Adaptation

Project description:Iron Drives Eosinophil Differentiation in Allergic Airway Inflammation through Mitochondrial Metabolic Adaptation

| PRJNA1082691 | ENA

Microarray analysis on RNA from lung eosinophil subpopulation from naive or HDM-treated mice using Affymetrix Mouse Gene 2.0 ST

Project description:As opposed to their well-characterized contributions to inflammatory processes, tissue eosinophils are now also thought to contribute to immune homeostasis at mucosal sites such as the gut. Yet, whether such steady-state eosinophils exist in the lung is currently unclear. In this project, we identified and characterized lung resident eosinophil and also studied what happen to these cell during a mouse model of allergic inflammation (House dust mite (HDM) exact administrations). We compared the transcriptional profile of lung resident eosinophil from naive mice (rEOS ss) or from HDM-treated mice (rEOS i) and of inflammatory eosinophil (iEOS) from HDM-treated mice.

2016-06-07 | E-MTAB-4084 | biostudies-arrayexpress

Diesel exhaust particles Enhance Monocyte Recruitment, Accelerating Allergic Airway Inflammation

Project description:Diesel exhaust particles Enhance Monocyte Recruitment, Accelerating Allergic Airway Inflammation

| PRJNA1196090 | ENA

DJ-1 governs airway progenitor cell/eosinophil interactions to promote allergic inflammation

Project description:DJ-1 is an antioxidant protein known to regulate mast cell mediated allergic response, but its role in airway eosinophilic interactions and allergic inflammation is not known.

2023-12-01 | GSE207415 | GEO

Comprehensive DNA Microarray Analysis for the Gene Sets Involved in Allergic Reaction by Allergic Effector Cells

Project description:Mast cells, basophils, and eosinophils play an important role in allergic disorders as effector cells. These cells secrete abundant serine proteases as well as chemical mediators and cytokines. Various serine proteases including SLPI are also important for to regulate an allergic response in these effector cells, although the expression profiles and functions of these proteases still remain unclear. We carried out DNA microarrays to clarify the role of SLPI in allergic responses.

2017-12-21 | GSE87638 | GEO

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