COMPARISON OF PATHOGENESIS OF P. BERGHEI INFECTION IN MOUSE AND RAT MODELS

Q4 Medicine
V. Chin, W. Chong, N. Nordin, TzeYan Lee, Zakaria Zainul Amiruddin, H. Hassan, R. Basir
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Abstract

Background: The cytokine cascade in the immunopathogenesis of malaria infection had been widely studied. However, their specific association with survival and severe infection remained obscure. Methods: The study investigated the cytokine profiles and histopathological features of malaria in the severe infection and survival models by using male ICR mice and male Sprague Dawley rats respectively. Results: The severe model, the infected ICR mice, exhibited a high parasitemia with 100% mortality after peak parasitemia at day 5 post-infection. The survival model, the infected Sprague Dawley rats, showed mild parasitemia with full recovery by day 14 of infection. Both severe and survival models showed similar histopathological severity during peak parasitemia. The severe model produced highly elevated levels of proinflammatory cytokines, TNF-α and IL-1α, and low levels of the anti-inflammatory cytokine, IL-4; while the survival model showed low levels of TNF-α and IL-1α with high levels of IL-4. Conclusion: There were differences in the pathogenesis of the severe and survival models of malaria infection. These could be a basis for immunotherapy of malaria in the future.
伯氏杆菌感染小鼠和大鼠模型的发病机制比较
背景:细胞因子级联在疟疾感染免疫发病机制中的作用已被广泛研究。然而,它们与生存和严重感染的具体联系仍然不清楚。方法:分别以雄性ICR小鼠和雄性Sprague Dawley大鼠为研究对象,研究重度感染模型和存活模型中疟疾的细胞因子谱和组织病理学特征。结果:重度模型感染的ICR小鼠在感染后第5天出现高寄生率,死亡率为100%。生存模型感染的大鼠表现为轻度寄生虫血症,感染后第14天完全恢复。严重模型和生存模型在寄生高峰期间显示相似的组织病理学严重程度。重度模型促炎细胞因子TNF-α、IL-1α水平高,抗炎细胞因子IL-4水平低;生存模型小鼠TNF-α、IL-1α水平低,IL-4水平高。结论:疟疾感染的发病机制和生存模式存在差异。这些可能是未来疟疾免疫治疗的基础。
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CiteScore
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