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Chikungunya virus infection disrupts lymph node lymphatic endothelial cell composition and function via MARCO
Cormac J Lucas1,2, Ryan M Sheridan2, Glennys V Reynoso3
1Department of Immunology & Microbiology and.
Insights
Chikungunya virus (CHIKV) infection disrupts lymph node organization by targeting lymphatic endothelial cells (LECs). CHIKV-MARCO interactions accelerate inflammation and impair crucial LEC functions like antigen acquisition.
Area of Science:
- Immunology
- Virology
- Cell Biology
Background:
- Chikungunya virus (CHIKV) infection disrupts draining lymph node (dLN) organization.
- This disruption includes B cell relocalization, loss of B cell-T cell borders, and lymphocyte depletion.
- Inflammatory myeloid cells infiltrate the lymph node during CHIKV infection.
Purpose of the Study:
- To investigate the early interactions between CHIKV and lymphatic endothelial cells (LECs) within the lymph node.
- To understand how these interactions influence the lymph node's inflammatory response and overall function during infection.
Main Methods:
- Tracking CHIKV RNA accumulation in MARCO-expressing LECs in LN sinuses.
- Analyzing gene expression changes in LN stromal cells.
- Assessing the impact of CHIKV-MARCO interactions on inflammatory responses and myeloid cell recruitment.
- Quantifying LEC numbers and evaluating antigen acquisition by LECs during CHIKV infection.
Main Results:
- CHIKV RNA accumulated in MARCO-expressing LECs in floor and medullary LN sinuses within 24 hours.
- Viral RNA accumulation triggered antiviral and inflammatory gene programs in LN stromal cells.
- CHIKV-MARCO interactions accelerated inflammatory responses and myeloid cell recruitment.
- CHIKV infection led to a decrease in floor and medullary LECs and reduced their antigen acquisition function.
Conclusions:
- LECs are early targets of CHIKV infection in the lymph node.
- CHIKV-MARCO interactions drive lymph node inflammation and dysfunction.
- Impaired LEC function compromises crucial immune surveillance mechanisms during CHIKV infection.
Abstract:
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 found that, during the first 24 hours of infection, CHIKV RNA accumulated 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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