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Differences in cytokine and chemokine profiles in cerebrospinal fluid caused by the etiology of cryptococcal meningitis and tuberculous meningitis in HIV patients
Clinical & Experimental Immunology ( IF 3.4 ) Pub Date : 2021-07-21 , DOI: 10.1111/cei.13644
Lijun Xu 1, 2 , Yufan Xu 1, 3 , Yanghao Zheng 1, 4 , Xiuming Peng 5 , Zongxing Yang 6 , Qing Cao 1, 2 , Dairong Xiang 1, 2 , Handan Zhao 1, 4
Affiliation  

The roles of cytokines and chemokines in HIV-associated cryptococcal meningitis (HCM) and HIV-associated tuberculous meningitis (HTBM) are debatable. In sum, 34 HIV-infected patients without meningitis, 44 HCM patients and 27 HTBM patients were enrolled for study. The concentrations of 22 cytokines/chemokines in cerebrospinal fluid (CSF) were assayed at admission. Principal component analysis (PCA), Pearson’s and logistic regression analyses were used to assess the role of cytokines/chemokines in HCM and HTBM. We found the levels of T helper (Th)17, Th1 [interleukin (IL)-12p40, interferon (IFN)-γ, tumor necrosis factor (TNF)-α and TNF-β and Th2 (IL-2/4/5/6/10)] cytokines were elevated in patients with meningitis compared with those in HIV-infected patients without central nervous system (CNS) infection. Furthermore, the IL-1Ra, IL-12p40, IL-17α and monocyte chemotactic protein-1 (MCP-1) levels were higher in HCM patients, while the IFN-γ, regulated upon activation, normal T cell expressed and secreted (RANTES) and interferon-inducible protein-10 (IP)-10 levels were higher in HTBM patients. Elevated CSF concentrations of IL-17a, TNF-β, IL-5, IL-12p40 and IL-1Rα were closely related to meningitis, but elevated IP-10, MCP-1, RANTES and IFN-γ levels and CSF white blood cells (WBCs) were protective factors against HCM. Our study suggested that HIV-infected patients with low CSF WBCs have a high risk of HCM. Th1, Th2 and Th17 cytokines/chemokines mediate differences in the pathogenesis of HCM and TBM. Overexpressed proinflammatory MCP-1, RANTES, IFN-γ and IP-10 in CSF are protective factors against HCM but not HTBM.

中文翻译:

HIV患者隐球菌性脑膜炎和结核性脑膜炎病因引起的脑脊液细胞因子和趋化因子谱差异

细胞因子和趋化因子在 HIV 相关隐球菌脑膜炎 (HCM) 和 HIV 相关结核性脑膜炎 (HTBM) 中的作用是有争议的。总之,34 名 HIV 感染的无脑膜炎患者、44 名 HCM 患者和 27 名 HTBM 患者被纳入研究。入院时测定脑脊液 (CSF) 中 22 种细胞因子/趋化因子的浓度。主成分分析 (PCA)、Pearson 和逻辑回归分析用于评估细胞因子/趋化因子在 HCM 和 HTBM 中的作用。我们发现了 T 辅助因子 (Th)17、Th1 [白介素 (IL)-12p40、干扰素 (IFN)-γ、肿瘤坏死因子 (TNF)-α 和 TNF-β 和 Th2 (IL-2/4/5) 的水平/6/10)] 与没有中枢神经系统 (CNS) 感染的 HIV 感染患者相比,脑膜炎患者的细胞因子升高。此外,IL-1Ra、IL-12p40、HCM 患者的 IL-17α 和单核细胞趋化蛋白 1 (MCP-1) 水平较高,而激活后调节的 IFN-γ、正常 T 细胞表达和分泌 (RANTES) 和干扰素诱导蛋白 10 (IP) HTBM 患者的-10 水平较高。脑脊液中 IL-17a、TNF-β、IL-5、IL-12p40 和 IL-1Rα 浓度升高与脑膜炎密切相关,但 IP-10、MCP-1、RANTES 和 IFN-γ 水平以及脑脊液白细胞升高(WBC) 是 HCM 的保护因素。我们的研究表明,低 CSF WBC 的 HIV 感染患者发生 HCM 的风险很高。Th1、Th2 和 Th17 细胞因子/趋化因子介导 HCM 和 TBM 发病机制的差异。脑脊液中过表达的促炎性 MCP-1、RANTES、IFN-γ 和 IP-10 是针对 HCM 而不是 HTBM 的保护因子。
更新日期:2021-09-17
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