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Local immune dysregulation and subsequent inflammatory response contribute to pulmonary edema caused by Enterovirus
Tiantian Sun1, Dong Li1, Xinchen Dai2
1Department of Epidemiology, College of Public Health, Zhengzhou University, Zhengzhou, China.
Abstract:
Pulmonary edema that comes on suddenly is the leading cause of mortality in hand-foot-and-mouth disease (HFMD) patients; however, its pathogenesis is still largely unclear. A range of research suggest immunopathogenesis during the occurrence of pulmonary edema in severe HFMD patients. Herein, to investigate the potential mechanism of immune dysregulation in the development of pulmonary edema upon Enterovirus (EV) infection, we established mouse infection models for Enteroviruses (EVs) including Coxsackievirus (CV) A6, Enterovirus A71 (EVA71), and CVA2 exhibiting a high incidence of pulmonary edema. We found that EVs infection induced an immune system disorder by reducing the numbers of pulmonary and circulatory T cells, B cells, macrophages, and monocytes and increasing the numbers of lung neutrophils, myeloid-derived suppressor cells (MDSCs), and activated T cells. In addition, the concentrations of C-X-C motif chemokine ligand 1 (CXCL-1), tumor necrosis factor-alpha, monocyte chemoattractant protein-1, and interleukin 6 were increased in EV-infected lungs. Moreover, we found that EVs replication in mice lungs lead to apoptosis of lung cells and degradation of tight junction proteins. In conclusion, EVs infection likely triggered a complexed immune defense mechanism and caused dysregulation of innate immune cells (MDSCs, neutrophils, monocytes, and macrophages) and adaptive cellular immunity (B cells, T cells). This dysregulation increased the release of cytokines and other inflammatory factors from activated immune-related cells and caused lung barrier damage and pulmonary edema.
Insights
Sudden pulmonary edema in severe hand-foot-and-mouth disease (HFMD) is linked to Enterovirus (EV) infection. EVs disrupt immune cells, causing lung damage and fatal edema.
Area of Science:
- * Virology
- * Immunology
- * Pathology
Background:
- * Sudden pulmonary edema is a major cause of mortality in severe hand-foot-and-mouth disease (HFMD).
- * The precise pathogenesis of pulmonary edema in HFMD remains largely unknown.
- * Emerging research suggests immunopathogenesis plays a role in severe HFMD-associated pulmonary edema.
Purpose of the Study:
- * To investigate the immune dysregulation mechanisms underlying pulmonary edema in Enterovirus (EV) infection.
- * To establish and utilize mouse models for studying EV-induced pulmonary edema.
Main Methods:
- * Established mouse infection models using Coxsackievirus (CV) A6, Enterovirus A71 (EVA71), and CVA2.
- * Analyzed changes in pulmonary and circulatory immune cell populations (T cells, B cells, macrophages, monocytes, neutrophils, myeloid-derived suppressor cells [MDSCs]).
- * Quantified inflammatory cytokine levels (CXCL-1, TNF-α, MCP-1, IL-6) and assessed lung cell apoptosis and tight junction protein integrity.
Main Results:
- * EV infection led to reduced pulmonary and circulatory T cells, B cells, macrophages, and monocytes.
- * Increased lung neutrophils, MDSCs, and activated T cells were observed.
- * Elevated levels of CXCL-1, TNF-α, MCP-1, and IL-6, along with lung cell apoptosis and tight junction protein degradation, were detected.
Conclusions:
- * EV infection triggers a complex immune response, leading to immune cell dysregulation.
- * Innate (MDSCs, neutrophils, monocytes, macrophages) and adaptive (B cells, T cells) immune cell imbalances contribute to disease progression.
- * This immune dysregulation promotes cytokine release, lung barrier damage, and ultimately, pulmonary edema.
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