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IgE-binding monocytes upregulate the coagulation cascade in allergic horses

ABSTRACT: IgE-binding monocytes upregulate the coagulation cascade in allergic horses

PROVIDER: PRJNA965804 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24389400_1.fastq.gz	Fastqsanger.gz
	SRR24389400_2.fastq.gz	Fastqsanger.gz
	SRR24389401_1.fastq.gz	Fastqsanger.gz
	SRR24389401_2.fastq.gz	Fastqsanger.gz
	SRR24389402_1.fastq.gz	Fastqsanger.gz

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IgE-binding monocytes upregulate the coagulation cascade in allergic horses

Project description:IgE-binding monocytes are a rare peripheral immune cell type involved in the allergic response through binding of IgE on their surface. IgE-binding monocytes are present in both healthy and allergic individuals. We performed RNA sequencing to ask how the function of IgE-binding monocytes differs in the context of allergy. Using a large animal model of allergy, equine Culicoides hypersensitivity, we compared the transcriptome of IgE-binding monocytes in allergic and non-allergic horses at two seasonal timepoints: (i) when allergic animals were clinical healthy, in the winter “Remission Phase”, and (ii) during chronic disease, in the summer “Clinical Phase”. Most transcriptional differences between allergic and non-allergic horses occurred only during the “Remission Phase”, suggesting principal differences in monocyte function even in the absence of allergen exposure. F13A1, a subunit of fibrinoligase, was significantly upregulated at both timepoints in allergic horses. This suggested a role for increased fibrin deposition in the coagulation cascade to promote allergic inflammation. IgE-binding monocytes also downregulated CCR10 expression in allergic horses during the “Clinical Phase”, suggesting a defect in maintenance of skin homeostasis, which further promotes allergic inflammation. Together, this transcriptional analysis provides valuable clues into the mechanisms used by IgE-binding monocytes in allergic individuals.

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IgE-binding monocytes upregulate the coagulation cascade in allergic horses.

Project description:IgE-binding monocytes are a rare peripheral immune cell type involved in the allergic response through binding of IgE on their surface. IgE-binding monocytes are present in both healthy and allergic individuals. We performed RNA sequencing to ask how the function of IgE-binding monocytes differs in the context of allergy. Using a large animal model of allergy, equine Culicoides hypersensitivity, we compared the transcriptome of IgE-binding monocytes in allergic and non-allergic horses at two seasonal timepoints: (i) when allergic animals were clinical healthy, in the winter "Remission Phase", and (ii) during chronic disease, in the summer "Clinical Phase". Most transcriptional differences between allergic and non-allergic horses occurred only during the "Remission Phase", suggesting principal differences in monocyte function even in the absence of allergen exposure. F13A1, a subunit of fibrinoligase, was significantly upregulated at both timepoints in allergic horses. This suggested a role for increased fibrin deposition in the coagulation cascade to promote allergic inflammation. IgE-binding monocytes also downregulated CCR10 expression in allergic horses during the "Clinical Phase", suggesting a defect in maintenance of skin homeostasis, which further promotes allergic inflammation. Together, this transcriptional analysis provides valuable clues into the mechanisms used by IgE-binding monocytes in allergic individuals.

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Project description:Diabetes is a multifactorial disorder and epigenetics changes are increasingly appreciated to influence the development of diabetic complications. Chromatin remodeling and histone acetylation are implicated in activation of the inflammatory response. Recently, histone deacetylase (HDAC) inhibitors (HDACi) have proved to reduce the severity of inflammatory diseases. We have previously shown that chromatin alterations regulated by HDACi in HepG2 cells stimulated by hyperglycemia reduced hepatic glucose production. In this study, we examined gene expression patterns using next generation sequencing. We show the pharmacological HDAC inhibitor VPA attenuates hyperglycemia induced gene expression, highlighting the relevance of complement and coagulation cascade. These findings reveal a novel mechanism of VPA protection against hyperglycemia induced hepatic gene expression changes, which might improve the therapeutic approaches for diabetes.

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