Department of Microbiology and Parasitology, Biosciences Center, Federal University of Rio Grande do Norte. Natal, Rio Grande do Norte, Natal, Rio Grande Do Norte, 59078-970, Brazil.
Edmond and Lily Safra International Institute of Neuroscience, Santos Dumont Institute, Macaiba, Rio Grande do Norte, Brazil.
Med Microbiol Immunol. 2023 Aug;212(4):279-290. doi: 10.1007/s00430-023-00771-y. Epub 2023 Jun 7.
Chikungunya disease (CHIKD) is an arbovirose that presents with high morbidity, mainly due to arthralgia. Inflammatory mediators including IL-6, IL-1β, GM-CSF and others have been implicated in the pathogenesis of CHIKD, whilst type I interferons can be associated with better outcomes. The role of pattern recognition receptors has been studied incompletely. Here, we evaluated the expression of RNA-specific PRRs, their adaptor molecules and downstream cytokines in acute CHIKD patients. Twenty-eight patients were recruited during the 3rd-5th day after the symptoms onset for clinical examination, peripheral blood collection and qRT-PCR analysis of PBMC to compare to the healthy control group (n = 20). We observed common symptoms of acute CHIKD, with fever, arthralgia, headache and myalgia being the most frequent. Compared with uninfected controls, acute CHIKV infection upregulates the expression of the receptors TLR3, RIG-I and MDA5, and also the adaptor molecule TRIF. Regarding cytokine expression, we found an upregulation of IL-6, IL-12, IFN-α, IFN-β and IFN-γ, which are related directly to the inflammatory or antiviral response. The TLR3-TRIF axis correlated with high expression of IL-6 and IFN-α. Interestingly, greater expression of MDA5, IL-12 and IFN-α was related to lower viral loads in CHIKD acute patients. Together, these findings help to complete the picture of innate immune activation during acute CHIKD, while confirming the induction of strong antiviral responses. Drawing the next steps in the understanding of the immunopathology and virus clearance mechanisms of CHIKD should be of utter importance in the aid of the development of effective treatment to reduce the severity of this debilitating disease.
基孔肯雅热(CHIKD)是一种虫媒病毒病,发病率高,主要表现为关节炎。白细胞介素 6(IL-6)、白细胞介素 1β(IL-1β)、粒细胞-巨噬细胞集落刺激因子(GM-CSF)等炎症介质被认为与 CHIKD 的发病机制有关,而 I 型干扰素可能与更好的预后相关。模式识别受体的作用尚未完全阐明。在这里,我们评估了急性 CHIKD 患者中 RNA 特异性 PRR、其衔接分子和下游细胞因子的表达。在症状出现后的第 3-5 天,招募了 28 名患者进行临床检查、外周血采集和 PBMC 的 qRT-PCR 分析,并与健康对照组(n=20)进行比较。我们观察到急性 CHIKD 的常见症状,发热、关节炎、头痛和肌痛最为常见。与未感染对照相比,急性 CHIKV 感染上调了 TLR3、RIG-I 和 MDA5 受体以及衔接分子 TRIF 的表达。关于细胞因子表达,我们发现 IL-6、IL-12、IFN-α、IFN-β 和 IFN-γ 的表达上调,这些与炎症或抗病毒反应直接相关。TLR3-TRIF 轴与 IL-6 和 IFN-α 的高表达相关。有趣的是,MDA5、IL-12 和 IFN-α 的更大表达与 CHIKD 急性患者的病毒载量较低相关。总之,这些发现有助于完善急性 CHIKD 期间固有免疫激活的图景,同时证实了强烈的抗病毒反应的诱导。了解 CHIKD 的免疫病理学和病毒清除机制的下一步应该是在开发有效治疗方法以减轻这种使人衰弱的疾病的严重程度方面非常重要。