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Single Cell Transcriptomics of Bone Marrow Derived Macrophages reveal Ccl5 as a marker of Direct IFNAR-independent Responses to DNA Sensing

ABSTRACT: Single Cell Transcriptomics of Bone Marrow Derived Macrophages reveal Ccl5 as a marker of Direct IFNAR-independent Responses to DNA Sensing

PROVIDER: PRJNA953992 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24119935_1.fastq.gz	Fastqsanger.gz
	SRR24119935_2.fastq.gz	Fastqsanger.gz
	SRR24119936_1.fastq.gz	Fastqsanger.gz
	SRR24119936_2.fastq.gz	Fastqsanger.gz
	SRR24119937_1.fastq.gz	Fastqsanger.gz

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Single Cell Transcriptomics of Bone Marrow Derived Macrophages reveal Ccl5 as a marker of Direct IFNAR-independent Responses to DNA Sensing

Project description:Bone marrow derived macrophages (BMDMs) are a common model for macrophage type 1 interferon responses. We used single cell RNA-seq (scRNA-seq) to identify direct responders for dsDNA sensing.

2023-06-07 | GSE229311 | GEO

Single cell transcriptomics of bone marrow derived macrophages reveals Ccl5 as a biomarker of direct IFNAR-independent responses to DNA sensing.

Project description:IntroductionThe type I interferon (IFN) response is an innate immune program that mediates anti-viral, anti-cancer, auto-immune, auto-inflammatory, and sterile injury responses. Bone marrow derived macrophages (BMDMs) are commonly used to model macrophage type I IFN responses, but the use of bulk measurement techniques obscures underlying cellular heterogeneity. This is particularly important for the IFN response to immune stimulatory double-stranded DNA (dsDNA) because it elicits overlapping direct and indirect responses, the latter of which depend on type I IFN cytokines signaling via the IFN alpha receptor (IFNAR) to upregulate expression of interferon stimulated genes (ISGs). Single cell transcriptomics has emerged as a powerful tool for revealing functional variability within cell populations.MethodsHere, we use single cell RNA-Seq to examine BMDM heterogeneity at steady state and after immune-stimulatory DNA stimulation, with or without IFNAR-dependent amplification.ResultsWe find that many macrophages express ISGs after DNA stimulation. We also find that a subset of macrophages express ISGs even if IFNAR is inhibited, suggesting that they are direct responders. Analysis of this subset reveals Ccl5 to be an IFNAR-independent marker gene of direct DNA sensing cells.DiscussionOur studies provide a method for studying direct responders to IFN-inducing stimuli and demonstrate the importance of characterizing BMDM models of innate immune responses with single cell resolution.

| S-EPMC10232813 | biostudies-literature

Analysis of transcriptional differences between ZIKV-infected Ifnar-/- and Ifnar+/- placentas

Project description:Purpose: While type I interferons (IFN) are important for control of viral replication, we see that, upon infection of Ifnar-/- females were crossed to Ifnar+/- males with ZIKV, only Ifnar+/- fetuses are resorbed or develop severe growth restriction. To identify how IFN may be altering placenta development, we performed RNAsequencing on infected and uninfected Ifnar-/- and Ifnar+/- placentas. Methods: Ifnar-/- females were crossed to Ifnar+/- males and infected intravaginally with Cambodian ZIKV at E5.5. Placentas were harvested from infected and uninfected pregnant dams at E10.5. Results/ Conclusions: Comparison of ZIKV-infected Ifnar-/- and Ifnar+/- shows an elevated interferon stimulated gene (ISG) signature in Ifnar+/- placentas but does not reveal any underlying developmental defects that may be causing defects in placenta development.

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Gene expression analysis of murine peritoneal macrophages deficient for SAMHD1 and IFNAR

Project description:To investigate the contribution of type-1 IFN signalling to the upregulation of IFN- stimulated genes in SAMHD1-deficient cells, we performed global gene expression analysis of SAMHD1-deficient IFNAR-/- macrophages. Peritoneal macrophages from ten SAMHD1-deficient IFNAR-/- and six SAMHD1-deficient controls were FACS sorted. RNA was subjected to next generation mRNA sequencing.

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dsRNA IP of Coronavirus Infected IFNAR-/- BMDMs

Project description:RNA-sequencing data of mock, wild-type, and EndoUmut MHV A59 infected IFNAR-/- bone-marrow derived macrophages. RNA was isolated at 6 hours post infection and immunoprecipitated with anti-dsRNA antibody to determine which RNA are forming a dsRNA epitope during viral infection. RNAs were mapped to C57Bl/6 Mouse genome or MHV-A59 genome (Genbank accession # AY910861).

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Cancer-associated fibroblast-derived CCL5 promotes cisplatin resistance in neuroendocrine prostate cancer

Project description:Chemoresistance remains a significant challenge in the treatment of neuroendocrine prostate cancer (NEPC), a highly aggressive and lethal subtype of prostate cancer. Here, we identify a tumor-stromal interaction mediated by the CCL5/CCR5 signaling axis that drives cisplatin resistance. Cisplatin-induced DNA damage promotes a cGAS-STING–dependent senescence program in cancer-associated fibroblasts (CAFs), resulting in the secretion of CCL5, a key senescence-associated secretory phenotype factor. CAF-derived CCL5 binds to CCR5 on tumor cells, promoting the formation of a CCR5/β-arrestin1/p85 complex that activates the PI3K/AKT signaling pathway. This activation enhances DNA repair, protecting tumor cells from cisplatin-induced apoptosis. Pharmacologic inhibition of the CCL5/CCR5 pathway using maraviroc, an FDA-approved CCR5 antagonist, sensitizes NEPC cells to cisplatin treatment and significantly prolongs survival in an NEPC mouse model. These findings establish the CCL5/CCR5 axis as a critical mediator of tumor-stromal crosstalk and provide a promising therapeutic strategy for overcoming chemoresistance in NEPC.

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Gene expression analysis of murine peritoneal macrophages deficient for SAMHD1 and IFNAR

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CCL5 promotes angiotensin II-induced cardiac remodeling through regulation of platelet-driven M2 macrophage polarization

Project description:Aims: Platelet activation plays a critical role in the pathogenesis of cardiovascular disease and inflammation, primarily through interactions with macrophages. CCL5, a chemokine stored in platelet α-granules, is released upon platelet activation. The present study determines the specific role of CCL5 in modulating platelet function, platelet-mediated macrophage polarization, and hypertensive cardiac remodelin. Conclusion: These findings underscore the detrimental role of CCL5-mediated platelet activation in triggering inflammatory responses and promoting M2 macrophage polarization during hypertensive cardiac remodeling, revealing the molecular mechanism by which CCL5 facilitates platelet-derived TGF-β1 signaling via NF-κB activation. These results elucidate the crosstalk between platelets and macrophages that exacerbates cardiac remodeling and highlight CCL5 as a potential therapeutic target for reducing inflammation and cardiac injury.

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