Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

CGRP-Related Neuropeptide Adrenomedullin 2 Promotes Tissue-Protective ILC2 Responses and Limits Intestinal Inflammation

ABSTRACT: CGRP-Related Neuropeptide Adrenomedullin 2 Promotes Tissue-Protective ILC2 Responses and Limits Intestinal Inflammation

PROVIDER: PRJNA1130984 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other
	SRR29686278_1.fastq.gz	Fastqsanger.gz
	SRR29686278_2.fastq.gz	Fastqsanger.gz
	SRR29686279_1.fastq.gz	Fastqsanger.gz
	SRR29686279_2.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 13

Similar Datasets

Neuropeptide CGRP limits ILC2 responses and constrains type 2 inflammation

Project description:Innate and adaptive lymphocytes work in concert to maintain tissue homeostasis and to mediate host defense at mucosal barriers. Herein, we used single cell analysis to show substantial diversity of gene expression in ILCs and T helper cells during a helminth infection in the lung. Notably, we found that the Calca gene, which is spliced to generate the neuropeptide CGRP, was selectively transcribed in ILC2s and Th2 cells in an activation dependent manner. The Calca locus acquired chromatin accessibility at the ILC2 precursor stage and is pre-programmed for rapid production of CGRP upon ILC2 activation. CGRP globally antagonized actions of neuromedin U (NMU) and the alarmin IL-33. However, CGRP selectively acted in concert with NMU and IL-33 to promote IL-5 expression, but not IL-13. The complex interplay among neuropeptides and alarmin fine-tunes type 2 immune responses and will undoubtedly become more relevant as therapeutic neuropeptide blockade advances in the clinic.

2019-06-25 | GSE131996 | GEO

Project description:Neuro-immune circuits regulate innate and adaptive immunity at barrier surfaces, however the differential impact of these circuits on proinflammatory versus tissue-protective responses remains poorly defined. We identify that enteric neurons produce CGRP-related adrenomedullin 2 (ADM2), and identify a previously unrecognized role for the ADM2-ADM2 receptor pathway in promoting intestinal tissue-protective functions of group 2 innate lymphoid cells (ILC2s). Genomic or ILC2-intrinsic deletion of ADM2 receptor subunits resulted in a significant reduction in tissue-protective ILC2 responses, defective amphiregulin (AREG) production and increased susceptibility to intestinal damage and inflammation. Conversely, therapeutic delivery of recombinant ADM2 elicited tissue-protective AREG production in ILC2s and limited intestinal inflammation. Expression of genes encoding human ADM2 receptor (CALCRL and RAMP3) was altered in IBD patients and associated with reduced expression of AREG in ILC2s. Collectively, these findings identify that the ADM2-ADM2 receptor pathway can promote tissue-protective functions of ILC2s in the context of intestinal damage and inflammation.

2025-06-25 | GSE271362 | GEO

Neuropeptide CGRP limits ILC2 responses and constrains type 2 inflammation

Project description:Neuropeptide CGRP limits ILC2 responses and constrains type 2 inflammation

| PRJNA545529 | ENA

Comprehensive transcriptional atlas of intestinal immune cells reveals that neuropeptide α-CGRP orchestrates ILC2 responses

Project description:Comprehensive transcriptional atlas of intestinal immune cells reveals that neuropeptide α-CGRP orchestrates ILC2 responses

| PRJNA514064 | ENA

Hypoxia Induces Lung Inflammation and Immunity by ILC2 through Stimulating Adrenomedullin from Epithelial Cells

Project description:Hypoxia contributes to airway inflammation and remodeling in several lung diseases; however, exactly how hypoxic pulmonary epithelium regulates allergic inflammation remains to be fully characterized. Here we report that conditional deletion of the E3 ubiquitin ligase VHL in lung epithelial cells resulted in exacerbated type 2 responses accompanied by selective increase of group 2 innate lymphoid cells (ILC2s) at steady state and following inflammation or helminth infection. Ablation of expression of the hypoxia-inducible factor 2 (HIF2a significantly reversed VHL-mediated ILC2 activation. VHL deficiency in lung epithelial cells caused the increased expression of the peptide hormone adrenomedullin (ADM), and our data suggest HIF2a controls Adm expression. ADM directly promoted ILC2 activation both in vitro and in vivo. Our findings indicate that the hypoxic response mediated by the VHL-HIF2a axis is critical for control of pulmonary type 2 responses by increasing ADM expression in lung epithelia causing ILC2 activation.

2022-05-04 | GSE197007 | GEO

Expression Data from fracture calli of alpha-CGRP deficient mice

Project description:alpha-CGRP is a neuropeptide that is also expressed in the fracture callus during bone regeneration. Our aim was to evaluate the role of alpha-CGRP in the context of fracture healing. Therefore we investigated the effect of alpha-CGRP deficiency on fracture callus formation. We used microarray analysis to compare the global gene expression of fracture calli from alpha-CGRP deficient mice and WT mice.

2020-09-02 | GSE148720 | GEO

PAC1 constrains type II inflammation through promotion of CGRP signaling in ILC2s [scRNA-seq]

Project description:Dysfunction of group II innate lymphoid cells (ILC2s) plays an important role in the development of type II inflammation-related diseases such as asthma and pulmonary fibrosis. Notably, neural signals are increasingly recognized as pivotal regulators of ILC2s. However, how ILC2s intrinsically modulate their responsiveness to these neural signals is still largely unknown. Here, using single-cell RNA sequencing and bulk mRNA sequencing, we report that the immune regulatory molecule PAC1 (phosphatase of activated cells 1) selectively promotes the signaling of neuropeptide CGRP (calcitonin gene-related peptide) in ILC2s. Moreover, PAC1 is necessary for ensuring the expression of CGRP-response genes by influencing chromatin accessibility. In summary, our study demonstrates that PAC1 is an important regulator of ILC2 responses and we propose that PAC1 is a potential target for therapeutic interventions of type II inflammation-related diseases.

2024-09-29 | GSE272724 | GEO

PAC1 constrains type II inflammation through promotion of CGRP signaling in ILC2s [RNA-seq]

2024-09-29 | GSE272723 | GEO

PAC1 constrains type II inflammation through promotion of CGRP signaling in ILC2s [FastATAC-seq]

2024-09-29 | GSE272722 | GEO

Calcitonin gene related peptide negatively regulates alarmin-driven type 2 innate lymphoid cell responses

Project description:Neuroimmune interactions have emerged as critical modulators of allergic inflammation, and type 2 innate lymphoid cells (ILC2s) are an important cell type for mediating these interactions. Here, we show that ILC2s expressed both the neuropeptide CGRP (Calcitonin Gene-Related Peptide) and its receptor. CGRP potently inhibited alarmin-driven type 2 cytokine production and proliferation by lung ILC2s both in vitro and in vivo. CGRP induced marked changes in ILC2 expression programs in vivo and in vitro, attenuating alarmin-driven proliferative and effector responses. A distinct subset of ILCs scored highly for a CGRP-specific gene signature after in vivo alarmin stimulation, suggesting CGRP regulated this response. Finally, we observed increased ILC2 proliferation and type 2 cytokine production and exaggerated responses to alarmins in mice lacking the CGRP receptor. Together, these data indicate that endogenous CGRP is a critical negative regulator of ILC2 responses in vivo.

2019-10-08 | GSE136154 | GEO