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

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

PROVIDER: PRJNA561400 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10011035_1.fastq.gz	Fastqsanger.gz
	SRR10011035_2.fastq.gz	Fastqsanger.gz
	SRR10011036_1.fastq.gz	Fastqsanger.gz
	SRR10011036_2.fastq.gz	Fastqsanger.gz
	SRR10011037_1.fastq.gz	Fastqsanger.gz

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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

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 calcitonin gene-related peptide (CGRP) 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 as well as 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.

| S-EPMC7076585 | biostudies-literature

Transcriptomics Changes of Calcitonin Gene-related Peptide in Mitigating Lipopolysaccharide-induced Septic Cardiomyopathy

Project description:Septic cardiomyopathy (SCM) is the predominant cause of death in sepsis patients with undefined mechanism to date. Our study analyzed RNA sequencing (RNA-seq) data from rat heart tissue to discover key targets and potential pharmacological actions of the calcitonin gene-related peptide (CGRP) against SCM. A lipopolysaccharide-induced SCM model was established in rats (LPS 10 mg/kg, intraperitoneal (i.p.)). Thereafter, the myocardial tissues from the three groups of rats (Ctrl group, LPS group, and CGRP group) (n=5) were extracted and underwent RNA-seq, followed by bioinformatics analyses. Our findings suggest a basis for finding potential targets for CGRP in the treatment of SCM.

2024-11-06 | GSE266124 | GEO

IL-33-activated calcitonin gene-related peptide-producing memory Th2 cells co-operate with somatosensory neurons to induce conjunctival itch

Project description:Allergic conjunctivitis is a chronic inflammatory disease that is characterized by severe itch in the conjunctiva; but how neuro-immune interactions shape the pathogenesis of severe itch remains unclear. We identified a subset of memory-type pathogenic Th2 cells that preferentially expressed Il1rl1-encoding ST2 and Calca-encoding calcitonin gene-related peptide (CGRP) in the inflammatory conjunctiva using a single-cell analysis. The IL-33-ST2 axis in memory Th2 cells controlled the axonal elongation of the peripheral sensory C-fiber and the induction of severe itch. Pharmacological blockade and genetic deletion of CGRP signaling in vivo attenuated scratching behavior. The analysis of giant papillae from patients with severe allergic conjunctivitis revealed ectopic lymphoid structure formation with the accumulation of IL-33-producing epithelial cells and CGRP-producing pathogenic CD4+ T cells accompanied by peripheral nerve elongation. Thus, the IL-33-ST2-CGRP axis directs severe itch with neuro-reconstruction in the inflammatory conjunctiva and is a potential therapeutic target for severe itch in allergic conjunctivitis.

2022-05-20 | GSE203217 | GEO

Transcriptomics Changes of Calcitonin Gene-related Peptide in Mitigating Lipopolysaccharide-induced Septic Cardiomyopathy

Project description:Transcriptomics Changes of Calcitonin Gene-related Peptide in Mitigating Lipopolysaccharide-induced Septic Cardiomyopathy

| PRJNA1105931 | ENA

Calcitonin controls bone formation by inhibiting the release of sphingosine 1-phosphate from osteoclasts

Project description:The hormone calcitonin (CT) is primarily known for its pharmacologic action as an inhibitor of bone resorption, yet CT-deficient mice display increased bone formation. These findings raised the question about the underlying cellular and molecular mechanism of CT action. Here we show that either ubiquitous or osteoclast-specific inactivation of the murine CT receptor (CTR) causes increased bone formation. CT negatively regulates the osteoclast expression of Spns2 gene, which encodes a transporter for the signaling lipid sphingosine 1-phosphate (S1P). CTR-deficient mice show increased S1P levels, and their skeletal phenotype is normalized by deletion of the S1P receptor S1P3. Finally, pharmacologic treatment with the non-selective S1P receptor agonist FTY720 causes increased bone formation in wildtype, but not in S1P3-deficient mice. This study redefines the role of CT in skeletal biology, confirms that S1P acts as an osteoanabolic molecule in vivo, and provides evidence for a pharmacologically exploitable crosstalk between osteoclasts and osteoblasts. Osteoclasts of wildtype and Calcr-/- C57Bl/6 mice were treated with Calcitonin and compared to the non-treated osteoclasts of wildtype or Calcr-/- mice, respectively.

2014-10-19 | E-GEOD-60761 | biostudies-arrayexpress

Sensory neurons expressing calcitonin gene-related peptide regulate adaptive thermogenesis and diet-induced obesity

Project description:Sensory neurons expressing calcitonin gene-related peptide regulate adaptive thermogenesis and diet-induced obesity

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Calcitonin gene-related peptide promotes reparative function of interleukin-4 educated human macrophages via COX1/PGD2 signalling

Project description:Calcitonin gene-related peptide promotes reparative function of interleukin-4 educated human macrophages via COX1/PGD2 signalling

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RNA-binding protein RBM3 negatively regulates innate lymphoid cells (ILCs) and lung inflammation

Project description:RNA-binding protein RBM3 negatively regulates innate lymphoid cells (ILCs) and lung inflammation

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Calcitonin gene-related peptide promotes reparative function of interleukin-4 educated human macrophages via COX1/PGD2 signalling

Project description:Interleukin-4 activated human macrophages (M(IL4) promote epithelial wound healing and exert an anti-colitic effect. Blood monocyte-derived M(IL4)s from healthy donors and individuals with Crohn’s disease had increased mRNA expression of the calcitonin gene-related peptide (CGRP) receptor chain, RAMP1, suggesting neural modulation of the M(IL4)s function. Thus, human (MIL4)s were treated with CGRP and the cells' phagocytic, epithelial wound repair and anti-colitic functions were assessed. M(IL4,CGRP)s had increased mannose receptor (CD206) and FcgRIIa (CD32a) mRNA expression, a subtle, but significant increase in phagocytosis, and decreased production of CXCL1, CCL3, CCL4, CCL5 and CXCL9 following exposure to E. coli. When delivered systemically (106 cells, ip.) to oxazolone-treated rag1-/- mice, M(IL4,CGRP) had an anti-colitic effect superior to M(IL4)s from the same healthy blood donor. The human colon CaCo2 epithelial cell line in an in vitro wounding model revealed that conditioned medium (CM) from M(IL4,CGRP) had increased amounts of TGFb and increased wound-healing capacity compared to matched M(IL4)-CM. Moreover, M(IL4,CGRP)s displayed increased cyclooxygenase (COX)-1 and prostaglandin D2, and CM from M(IL4,CGRP)s treated with indomethacin or SC-560 to inhibit COX1 activity failed to promote repair of wounded CaCo2 cell monolayers. These data confirm the human M(IL4)s’ anti-colitic effect that could be enhanced by the local availability of CGRP, which may be dependent, at least in part via macrophage COX1/PDG2 activity. Thus, neuronal input is revealed as an important local modifier capable of boosting the anti-colitic effect of autologous M(IL4) transfer to treat enteric inflammation

2024-09-30 | GSE242543 | GEO