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

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

PROVIDER: PRJNA1013899 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25992617_1.fastq.gz	Fastqsanger.gz
	SRR25992617_2.fastq.gz	Fastqsanger.gz
	SRR25992618_1.fastq.gz	Fastqsanger.gz
	SRR25992618_2.fastq.gz	Fastqsanger.gz
	SRR25992619_1.fastq.gz	Fastqsanger.gz

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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

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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.

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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.

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Project description:Nonhealing diabetic wounds, with persistent inflammation and damaged vasculature, have failed conventional treatments and require comprehensive interference. Here, inspired by tumor-associated macrophages (TAMs) that produce abundant immunosuppressive and proliferative factors in tumor development, we generate macrophages to recapitulate TAMs' reparative functions, by culturing normal macrophages with TAMs' conditional medium (TAMs-CM). These TAMs-educated macrophages (TAMEMs) outperform major macrophage phenotypes (M0, M1, or M2) in suppressing inflammation, stimulating angiogenesis, and activating fibroblasts in vitro. When delivered to skin wounds in diabetic mice, TAMEMs efficiently promote healing. Based on TAMs-CM's composition, we further reconstitute a nine-factor cocktail to train human primary monocytes into TAMEMsC-h , which fully resemble TAMEMs' functions without using tumor components, thereby having increased safety and enabling the preparation of autologous cells. Our study demonstrates that recapitulating TAMs' unique reparative activities in nontumor cells can lead to an effective cell therapeutic approach with high translational potential for regenerative medicine.

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