Pathogenesis of Enterovirus 71 Brainstem Encephalitis in Pediatric Patients: Roles of Cytokines and Cellular Immune Activation in Patients with Pulmonary Edema

Taiwan experienced several epidemics of enterovirus 71 (EV71) infections, which were associated with brainstem encephalitis (BE) and pulmonary edema (PE). To elucidate the role of immune mechanisms in the pathogenesis of BE caused by EV71 and its fatal complication, PE, we analyzed the laboratory fi...

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Published inThe Journal of infectious diseases Vol. 188; no. 4; pp. 564 - 570
Main Authors Wang, Shih-Min, Lei, Huan-Yao, Huang, Kao-Jean, Wu, Jing-Ming, Wang, Jen-Ren, Yu, Chun-Keung, Su, Ih-Jen, Liu, Ching-Chuan
Format Journal Article
LanguageEnglish
Published Chicago, IL The University of Chicago Press 15.08.2003
University of Chicago Press
Oxford University Press
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Summary:Taiwan experienced several epidemics of enterovirus 71 (EV71) infections, which were associated with brainstem encephalitis (BE) and pulmonary edema (PE). To elucidate the role of immune mechanisms in the pathogenesis of BE caused by EV71 and its fatal complication, PE, we analyzed the laboratory findings, cytokine, and immunophenotypes of 73 EV71-infected patients with BE. Patients were stratified by disease: PE (n=14), autonomic nervous system (ANS) dysregulation (n=25), and isolated BE (n=34). The mortality rate for PE was 64.3%. Leukocytosis and thrombocytosis were significantly more frequent among patients with PE. A significant elevation of plasma interleukin (IL)–10, IL-13, and interferon (IFN)–γ levels observed in patients with PE. Patients with PE also had lower circulating CD4+ T cells, CD8+ T cells, and natural killer (NK) cells. An extensive peripheral and central nervous system inflammatory response with abnormal IL-10, IL-13, and IFN-γ cytokine production and lymphocyte depletion appears to be responsible for the pathogenesis of EV71-associated PE
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ISSN:0022-1899
1537-6613
DOI:10.1086/376998