基孔肯雅病毒感染人类患者在极早期急性期引发的细胞因子和趋化因子。
Cytokines and chemokines triggered by Chikungunya virus infection in human patients during the very early acute phase.
作者信息
Tanabe Ithallo S B, Santos Elane C, Tanabe Eloiza L L, Souza Stephannie J M, Santos Fabio E F, Taniele-Silva Jamile, Ferro Jean F G, Lima Magliones C, Moura Adriana A, Anderson Leticia, Bassi Ênio J
机构信息
IMUNOREG-Grupo de Pesquisa em Regulação da Resposta Imune, Laboratório de Pesquisas em Virologia e Imunologia, Instituto de Ciências Biológicas e da Saúde, Universidade Federal de Alagoas, Maceió, Alagoas, Brazil.
Laboratório Central de Saúde Pública de Alagoas, Maceió, Alagoas, Brazil.
出版信息
Trans R Soc Trop Med Hyg. 2019 Nov 1;113(11):730-733. doi: 10.1093/trstmh/trz065.
BACKGROUND
The immune response against the Chikungunya virus (CHIKV) during the very early acute phase is not fully elucidated. Therefore we explored the cytokine and chemokine profile triggered by CHIKV in infected patients.
METHODS
Cytokines, chemokines and C5a anaphylatoxin were analysed in serum from CHIKV-infected patients during the viraemic phase (mean 2.97±1.27 d after illness onset) compared with a healthy group.
RESULTS
CHIKV-infected patients had a significant increase of interferon-α (IFN-α), interleukin-6 (IL-6), interleukin-8 (CXCL8/IL-8), interleukin-10 (IL-10), interferon-γ (IFN-γ), monokine induced by interferon-γ (CXCL9/MIG), monocyte chemoattractant protein-1 (CCL2/MCP-1), interferon-γ-induced protein-10 (CXCL10/IP-10) and complement C5a anaphylatoxin.
CONCLUSIONS
The very early acute immune response triggered against CHIKV leads to an increase in pro-inflammatory immune mediators such as IFN-γ and its induced chemokines, and a high level of C5a anaphylatoxin as a result of complement activation.
背景
基孔肯雅病毒（CHIKV）在极早期急性期的免疫反应尚未完全阐明。因此，我们探究了CHIKV在感染患者中引发的细胞因子和趋化因子谱。
方法
将CHIKV感染患者病毒血症期（发病后平均2.97±1.27天）血清中的细胞因子、趋化因子和C5a过敏毒素与健康组进行分析比较。
结果
CHIKV感染患者的α干扰素（IFN-α）、白细胞介素-6（IL-6）、白细胞介素-8（CXCL8/IL-8）、白细胞介素-10（IL-10）、γ干扰素（IFN-γ）、γ干扰素诱导的单核因子（CXCL9/MIG）、单核细胞趋化蛋白-1（CCL2/MCP-1）、γ干扰素诱导蛋白-10（CXCL10/IP-10）和补体C5a过敏毒素显著增加。
结论
针对CHIKV触发的极早期急性免疫反应导致促炎免疫介质如IFN-γ及其诱导的趋化因子增加，以及补体激活产生的高水平C5a过敏毒素。
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