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Alarmin-loaded extracellular lipid droplets induce airway neutrophil infiltration during type 2 inflammation

ABSTRACT: Alarmin-loaded extracellular lipid droplets induce airway neutrophil infiltration during type 2 inflammation

PROVIDER: PRJNA1030761 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26457923_1.fastq.gz	Fastqsanger.gz
	SRR26457923_2.fastq.gz	Fastqsanger.gz
	SRR26457924_1.fastq.gz	Fastqsanger.gz
	SRR26457924_2.fastq.gz	Fastqsanger.gz
	SRR26457925_1.fastq.gz	Fastqsanger.gz

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Alarmin-loaded extracellular lipid droplets induce airway neutrophil infiltration during type 2 inflammation

Project description:Group 2 innate lymphoid cells (ILC2s) play a crucial role in allergic diseases by coordinating a complex network of various effector cell lineages involved in type 2 inflammation. However, their function in regulating airway neutrophil infiltration, a deleterious symptom of severe asthma, remains unknown. Here, we observed ILC2-dependent neutrophil accumulation in the bronchoalveolar lavage fluid (BALF) of allergic mice models. Chromatography followed by proteomics analysis identified the alarmin high mobility group box-1 (HMGB1) in the supernatant of lung ILC2s initiated neutrophil chemotaxis. Genetic perturbation of Hmgb1 in ILC2s reduced BALF neutrophil numbers and alleviated airway inflammation. HMGB1 was loaded onto the membrane of lipid droplets (LDs) released from activated lung ILC2s. Genetic inhibition of LD accumulation in ILC2s significantly decreased extracellular HMGB1 abundance and BALF neutrophil infiltration. These findings unveil a previously uncharacterized extracellular LD-mediated immune signaling delivery pathway by which ILC2s regulate airway neutrophil infiltration during allergic inflammation.

2024-09-21 | GSE245964 | GEO

Elane mediates neutrophil infiltration into the brain and neuroinflammation

Project description:In CUMS mice, neutrophils can infiltrate brain parenchyma and induce neuroinflammatory responses. To identify potential mediators, we analyzed the gene expression profiles of bone marrow neutrophils from mice subjected to CUMS and compared them with those of control mice. Interestingly, among the genes notably associated with neutrophil functions were Elane and Mpo, the crucial granule proteins of neutrophils that mediate chronic inflammation. Our study demonstrated that neutrophil-specific Elane knockout reduced neutrophil infiltration into the brain parenchyma and alleviated neuroinflammation. Elane plays a critical role in modulating the influence of peripheral neutrophils on brain.

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Elane mediates neutrophil infiltration into the brain and neuroinflammation

Project description:Elane mediates neutrophil infiltration into the brain and neuroinflammation

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Engineered mesenchymal stromal cells with bispecific polyvalent peptides suppress excessive neutrophil infiltration and boost therapy

Project description:Excessive neutrophil infiltration can exacerbate inflammation and tissue damage, contributing to conditions like autoimmune disorders and liver diseases. Mesenchymal stromal cells (MSCs) share homing mechanisms with neutrophils, showing promise for treating such diseases. However, ex vivo expanded MSCs often suffer from reduced homing efficiency due to the loss of essential ligands. Here, we engineer MSCs with P-selectin and E-selectin targeting peptides, assembling them into bispecific polyvalent structures using DNA self-assembly technology. This modification allows engineered MSCs to compete with chemotactic neutrophils for selectin binding sites on endothelial cells. In a mouse model of acute liver failure, engineered MSCs effectively home to the damaged liver and significantly inhibit excessive neutrophil infiltration. The combination of inhibiting neutrophil infiltration and the MSCs’ inherent therapeutic properties lead to superior therapeutic outcomes. Single cell RNA sequencing reveals that engineered MSCs elevate the levels of Marco_macrophage which possess neutrophil-inhibitory effects. Our study offers a perspective for advancing MSC-based therapies in tissue repair.

2025-02-24 | GSE286317 | GEO

Integrated pathways for neutrophil recruitment and inflammation in leprosy

Project description:Neutrophil recruitment is pivotal to host defense against microbial infection, but also contributes to the immunopathology of disease. We investigated the mechanism of neutrophil recruitment in human infectious disease by bioinformatic pathways analysis of the gene expression profiles in the skin lesions of leprosy. In erythema nodosum leprosum (ENL), which occurs in patients with lepromatous leprosy (L-lep), and is characterized by neutrophil infiltration in lesions, the most overrepresented biologic functional group was “cell movement” including E-selectin, which was coordinately regulated with IL-1. In vitro activation of TLR2, upregulated in ENL lesions, triggered induction of IL-1, which together with IFN-, induced E-selectin expression on, and neutrophil adhesion to endothelial cells. Thalidomide, an effective treatment for ENL, inhibited this neutrophil recruitment pathway. The gene expression profile of ENL lesions comprised an integrated pathway of TLR2/FcR activation, neutrophil migration and inflammation, providing insight into mechanisms of neutrophil recruitment in human infectious disease. 6 ENL skin lesions and 7 Lepromatous leprosy skin lesions

2009-06-30 | E-GEOD-16844 | biostudies-arrayexpress

Parabacteroides produces acetate to alleviate heparanase-exacerbated acute pancreatitis through reducing neutrophil infiltration

Project description:Parabacteroides produces acetate to alleviate heparanase-exacerbated acute pancreatitis through reducing neutrophil infiltration

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Navarixin alleviates cardiac remodeling after myocardial infarction by decreasing neutrophil infiltration and the inflammatory response

Project description:Introduction: Coronary atherosclerotic heart disease is an important, worldwide burden on human health. Central muscle infarction is the most dangerous condition, has the highest mortality and disability rates, and is gradually becoming more common among young people. After myocardial infarction, neutrophils recruited to the infarcted area promote the myocardial inflammatory response by releasing proinflammatory factors and chemokines and release matrix metalloproteinases and myeloperoxidases that degrade the extracellular matrix and produce reactive oxygen species, resulting in irreversible myocardial damage and thereby promoting ventricular remodeling. Methods: In this study, we constructed a mouse model of myocardial infarction and utilized the CXCR2 receptor inhibitor navarixin (Nav) to reduce neutrophil recruitment after MI. Results: We observed that Nav improved cardiac function, reduced myocardial damage, reduced neutrophil infiltration, reduced inflammatory factor expression and improved cardiac fibrosis in mice. Through transcriptomic analysis, we found that Nav affects signaling pathways such as the innate immune response and the chemokine signaling pathway, thereby decreasing the inflammatory response by reducing neutrophil chemotaxis. Discussion: This study provides new insights for the use of CXCR2 inhibitors as new therapeutic options for myocardial infarction in the future.

2025-03-11 | GSE291292 | GEO

Neutrophil Extracellular Traps Mediate Acute Liver Failure in Regulation of miR-223/neutrophil Elastase Signaling in Mice

Project description:Marked enhancement of neutrophil infiltration of the liver is a hallmark of acute liver failure (ALF), a severe life-threatening disease with varying etiologies. However, the mechanisms underlying the regulation of neutrophil entry into the liver and their pathophysiological role during ALF development remain poorly characterized.

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Pitch Lake water droplets

Project description:Pitch Lake water droplets Raw sequence reads

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The alarmin interleukin-33 drives protective antiviral CD8+ T cell responses

Project description:Pathogen-associated molecular patterns decisively influence antiviral immune responses, whereas the contribution of endogenous signals of tissue damage, also known as “damage-associated molecular patterns” or “alarmins”, remains ill-defined. We show that interleukin-33 (IL-33), an alarmin released from necrotic cells, is necessary for potent CD8+ T cell (CTL) responses to replicating, prototypic RNA and DNA viruses in mice. IL-33 signaled through its receptor on activated CTLs, enhanced clonal expansion in a MyD88-dependent, CTL-intrinsic fashion, determined polyfunctional effector cell differentiation and was necessary for virus control. Moreover, recombinant IL-33 augmented vaccine-induced CTL responses. Radio-resistant cells of the splenic T cell zone produced IL-33, and efficient CTL responses required IL-33 from radio-resistant cells but not from hematopoietic cells. Thus, alarmin release by radio-resistant cells orchestrates protective antiviral CTL responses. 2 groups (wt vs. ST-/- P14 cells), 3 replicates per group.

2012-02-27 | E-GEOD-34392 | biostudies-arrayexpress

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