Neuroinflammation is associated with reduced SOCS2 and SOCS3 expression during intracranial HSV-1 infection

NEUROSCIENCE LETTERS

卷:736

Article

de Brito Toscano, Eliana Cristina¹  da Cunha Sousa, Larissa Fonseca²  Lima, Graciela Kunrath²  Mesquita, Leonardo Antunes³  Vilela, Marcia Carvalho⁸  Rodrigues, David Henrique⁸  Ferreira, Rodrigo Novaes²  Soriani, Frederico Marianetti⁴  Campos, Marco Antonio⁷  Kroon, Erna Geessien³  Teixeira, Mauro Martins⁵  de Miranda, Aline Silva²  Rachid, Milene Alvarenga¹  Teixeira, Antonio Lucio⁶ 

[1] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Patol Geral, Belo Horizonte, MG, Brazil

[2] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Morfol, Belo Horizonte, MG, Brazil

[3] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Microbiol, Belo Horizonte, MG, Brazil

[4] Univ Fed Minas Gerais, Inst Ciencias Biol, Dept Biol Geral, Belo Horizonte, MG, Brazil

[5] Univ Fed Juiz Fora, Inst Ciencias Biol, Dept Bioquim & Imunol, Juiz De Fora, Brazil

[6] Univ Texas Hlth Sci Ctr Houston, Neuropsychiat Program, Dept Psychiat & Behav Sci, Sch Med, Houston, TX 77030 USA

[7] Fiocruz Minas, Inst Rene Rachou, Belo Horizonte, MG, Brazil

[8] Univ Fed Juiz de Fora, Dept Ciencias Basicas & Vida, Juiz De Fora, Brazil

关键词: Encephalitis;    Apoptosis;    SOCS2;    SOCS3;    Brain inflammation;   

DOI  :  10.1016/j.neulet.2020.135295

来源: Elsevier

【 摘 要 】

Herpes simplex virus type 1 (HSV-1) is the main etiological agent of acute and sporadic encephalitis. Proteins of the suppressor of cytokine signaling (SOCS) family have shown to regulate the inflammation during HSV-1 infection in the brain. However, the effects of SOCS2 and SOCS3 in viral encephalitis remain unclear. The aim of the current study is to investigate the potential association between SOCS2, SOCS3, cytokines, and hippocampal damage, especially neuronal apoptosis, during acute intracranial HSV-1 infection in mice. Male C57BL/6 mice were infected by intracranial route with 102 plaque-forming units (PFU) inoculum of purified HSV-1. At three days post-infection (3 d.p.i.), mice were euthanized and their hippocampi were collected for histopathological analysis, immunohistochemical reaction against active caspase-3 and quantification of SOCS2, SOCS3 and cytokines (tumoral necrosis factor (TNF), interleukin (IL) 1 beta, IL-6, IL-10; interferon (IFN)-alpha, IFN-beta, IFN-gamma) mRNA expression. Infected mice exhibited neuronal loss and hemorrhagic focus in Cornu Ammonis (CA) region. The apoptotic index was higher in infected mice compared to controls. HSV-1 infection was associated with increased hippocampal expression of TNF, IL1-beta, IL-6 and IFN alpha/IFN beta and decreased expression of IL-10, IFN-gamma, SOCS2 and SOCS3. Our results suggest that down regulation of SOCS2 and SOCS3 contributes to a pro-inflammatory environment associated with hippocampal damage and neuronal apoptosis during acute HSV-1 infection in mice.

【 授权许可】

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