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Chikungunya virus infection disrupts lymph node lymphatic endothelial cell composition and function via MARCO

ABSTRACT: Chikungunya virus infection disrupts lymph node lymphatic endothelial cell composition and function via MARCO

PROVIDER: PRJNA1019315 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26130200_1.fastq.gz	Fastqsanger.gz
	SRR26130200_2.fastq.gz	Fastqsanger.gz
	SRR26130201_1.fastq.gz	Fastqsanger.gz
	SRR26130201_2.fastq.gz	Fastqsanger.gz
	SRR26130202_1.fastq.gz	Fastqsanger.gz

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Chikungunya virus infection disrupts lymph node lymphatic endothelial cell composition and function via MARCO

Project description:Infection with chikungunya virus (CHIKV) causes disruption of draining lymph node (dLN) organization, including paracortical relocalization of B cells, loss of the B cell-T cell border, and lymphocyte depletion that is associated with infiltration of the LN with inflammatory myeloid cells. Here, we find that during the first 24 h of infection, CHIKV RNA accumulates in MARCO-expressing lymphatic endothelial cells (LECs) in both the floor and medullary LN sinuses. The accumulation of viral RNA in the LN was associated with a switch to an antiviral and inflammatory gene expression program across LN stromal cells, and this inflammatory response, including recruitment of myeloid cells to the LN, was accelerated by CHIKV-MARCO interactions. As CHIKV infection progressed, both floor and medullary LECs diminished in number, suggesting further functional impairment of the LN by infection. Consistent with this idea, antigen acquisition by LECs, a key function of LN LECs during infection and immunization, was reduced during pathogenic CHIKV infection.

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MARCO+ lymphatic endothelial cells sequester arthritogenic alphaviruses in the draining lymph node and limit viral dissemination

Project description:While viremia in the vertebrate host is a critical determinant of arboviral reservoir competency, transmission efficiency, and disease severity, immune mechanisms that control arboviral viremia are poorly defined. Here, we identify critical roles for the scavenger receptor MARCO in controlling viremia during arthritogenic alphavirus infections in mice. Following subcutaneous inoculation, alphavirus particles drain via the lymph and are rapidly captured by MARCO+ lymphatic endothelial cells (LECs) in the draining lymph node (dLN), limiting viral spread to the bloodstream. Upon reaching the bloodstream, MARCO-expressing Kupffer cells in the liver remove circulating alphavirus particles, limiting viremia and further viral dissemination. MARCO-mediated accumulation of alphavirus particles in the lymph node and liver has important implications as viremia and viral tissue burdens are elevated in MARCO-/- mice and disease outcomes are more severe. These findings uncover a previously unrecognized pathogen scavenging role for LECs and improve our mechanistic understanding of viremia control during arboviral infections.

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MARCO+ lymphatic endothelial cells sequester arthritogenic alphaviruses in the draining lymph node and limit viral dissemination

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Project description:Purpose: The objective was to identify genes regulted by RANK signalling in lymph node lymphatic endothelial cells Method: Lymphatic endothelial cells were FACS sorted from peripheral lymph nodes of mice deficient for stromal RANKL (Ccl19 Cre Rankl flox/flox) versus littermate controls (Rankl flox/flox) and processed for bulk RNA sequencing Results: Upregulated and downregulated genes were identified

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Expression data for lymph node lymphatic endothelial cells and blood endothelial cells

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Project description:To gain additional insight into the role of MARCO in dendritic cell activation and function, we profiled transcriptomes of mouse splenic dendritic cells obtained from MARCO deficient mice and their wild type counterparts under resting and activating conditions. Pure dendritic cells from the spleens of WT and MARCO KO mice were cultured overnight in PBS or Lipopolysaccharide (LPS). Gene expression profiling was performed using Affymetrix platform.

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