Corilagin Interferes With Toll-Like Receptor 3-Mediated Immune Response in Herpes Simplex Encephalitis
Herpes simplex encephalitis (HSE) is the most common infectious disease of the central nervous system worldwide. However, the pathogenesis of HSE is not clear. Research has shown that the immune response mediated by the toll-like receptor 3 (TLR3) signaling pathway is essential to protect the centra...
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| Format: | Article |
| Language: | English |
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Frontiers Media S.A.
2019-04-01
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| Series: | Frontiers in Molecular Neuroscience |
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| Online Access: | https://www.frontiersin.org/article/10.3389/fnmol.2019.00083/full |
| _version_ | 1798046067788349440 |
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| author | Lu-Jun Li Shao-Jun Zhang Pan Liu You-Qin Wang Zhi-Lin Chen Yu-Jie Wang Jia-Bin Zhou Yuan-Jin Guo Lei Zhao |
| author_facet | Lu-Jun Li Shao-Jun Zhang Pan Liu You-Qin Wang Zhi-Lin Chen Yu-Jie Wang Jia-Bin Zhou Yuan-Jin Guo Lei Zhao |
| author_sort | Lu-Jun Li |
| collection | DOAJ |
| description | Herpes simplex encephalitis (HSE) is the most common infectious disease of the central nervous system worldwide. However, the pathogenesis of HSE is not clear. Research has shown that the immune response mediated by the toll-like receptor 3 (TLR3) signaling pathway is essential to protect the central nervous system against herpes simplex virus (HSV) infection. However, an excessive immune response may cause tissue damage accompanied by pathological changes. The aim of this study was to explore the molecular mechanism via which corilagin controls HSE through the TLR3 signaling pathway in vitro and in vivo. Cells and mice were pre-treated with polyriboinosinic polyribocytidylic acid [poly(I:C)] or HSV type 1, and then treated with corilagin. After treatment, the mRNA and protein levels of TLR3, TLR-like receptor-associated interferon factor (TRIF), tumor necrosis factor (TNF) receptor type 1-associated DEATH domain protein (TRADD), TNF receptor-associated factor (TRAF) 3 and 6, nuclear factor-kappa-B (NF-κB) essential modulator (NEMO), P38, and interferon regulatory factor 3 (IRF3) were decreased. Interleukin-6 (IL-6), TNF-α, and type 1 interferon-β were also decreased. When TLR3 expression was silenced or increased, corilagin still inhibited the expression of TLR3 and its downstream mediators. Hematoxylin-eosin (HE) staining and immunohistochemical examinations of mouse brain tissues revealed that corilagin lessened the degree of brain inflammation. Altogether, these results suggest that corilagin may regulate the immune response in HSE and relieve inflammatory injury by interfering with the TLR3 signaling pathway. |
| first_indexed | 2024-04-11T23:31:36Z |
| format | Article |
| id | doaj.art-b2444baab28f41c09fc6a19d46b4f8c8 |
| institution | Directory Open Access Journal |
| issn | 1662-5099 |
| language | English |
| last_indexed | 2024-04-11T23:31:36Z |
| publishDate | 2019-04-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Molecular Neuroscience |
| spelling | doaj.art-b2444baab28f41c09fc6a19d46b4f8c82022-12-22T03:57:07ZengFrontiers Media S.A.Frontiers in Molecular Neuroscience1662-50992019-04-011210.3389/fnmol.2019.00083432913Corilagin Interferes With Toll-Like Receptor 3-Mediated Immune Response in Herpes Simplex EncephalitisLu-Jun Li0Shao-Jun Zhang1Pan Liu2You-Qin Wang3Zhi-Lin Chen4Yu-Jie Wang5Jia-Bin Zhou6Yuan-Jin Guo7Lei Zhao8National & Local Joint Engineering Research Center of High-throughput Drug Screening Technology, State Key Laboratory of Biocatalysis and Enzyme Engineering, Hubei University, Wuhan, ChinaNational & Local Joint Engineering Research Center of High-throughput Drug Screening Technology, State Key Laboratory of Biocatalysis and Enzyme Engineering, Hubei University, Wuhan, ChinaSchool of Clinical Medicine, Hubei University of Chinese Medicine, Wuhan, ChinaRenmin Hospital of Hubei University of Medicine, The Postgraduate Training Center of Jinzhou Medical University, Shiyan, ChinaDepartment of Infectious Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Vascular Surgery, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Neurosurgery, Affiliated Hospital of Jining Medical University and Shangdong Provincial Key Laboratory of Stem Cells and Neuro-Oncology, Jining, ChinaDepartment of Neurology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaDepartment of Infectious Diseases, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, ChinaHerpes simplex encephalitis (HSE) is the most common infectious disease of the central nervous system worldwide. However, the pathogenesis of HSE is not clear. Research has shown that the immune response mediated by the toll-like receptor 3 (TLR3) signaling pathway is essential to protect the central nervous system against herpes simplex virus (HSV) infection. However, an excessive immune response may cause tissue damage accompanied by pathological changes. The aim of this study was to explore the molecular mechanism via which corilagin controls HSE through the TLR3 signaling pathway in vitro and in vivo. Cells and mice were pre-treated with polyriboinosinic polyribocytidylic acid [poly(I:C)] or HSV type 1, and then treated with corilagin. After treatment, the mRNA and protein levels of TLR3, TLR-like receptor-associated interferon factor (TRIF), tumor necrosis factor (TNF) receptor type 1-associated DEATH domain protein (TRADD), TNF receptor-associated factor (TRAF) 3 and 6, nuclear factor-kappa-B (NF-κB) essential modulator (NEMO), P38, and interferon regulatory factor 3 (IRF3) were decreased. Interleukin-6 (IL-6), TNF-α, and type 1 interferon-β were also decreased. When TLR3 expression was silenced or increased, corilagin still inhibited the expression of TLR3 and its downstream mediators. Hematoxylin-eosin (HE) staining and immunohistochemical examinations of mouse brain tissues revealed that corilagin lessened the degree of brain inflammation. Altogether, these results suggest that corilagin may regulate the immune response in HSE and relieve inflammatory injury by interfering with the TLR3 signaling pathway.https://www.frontiersin.org/article/10.3389/fnmol.2019.00083/fullcorilaginherpes simplex virus type 1inflammationsignaling pathwaytoll-like receptor 3 |
| spellingShingle | Lu-Jun Li Shao-Jun Zhang Pan Liu You-Qin Wang Zhi-Lin Chen Yu-Jie Wang Jia-Bin Zhou Yuan-Jin Guo Lei Zhao Corilagin Interferes With Toll-Like Receptor 3-Mediated Immune Response in Herpes Simplex Encephalitis Frontiers in Molecular Neuroscience corilagin herpes simplex virus type 1 inflammation signaling pathway toll-like receptor 3 |
| title | Corilagin Interferes With Toll-Like Receptor 3-Mediated Immune Response in Herpes Simplex Encephalitis |
| title_full | Corilagin Interferes With Toll-Like Receptor 3-Mediated Immune Response in Herpes Simplex Encephalitis |
| title_fullStr | Corilagin Interferes With Toll-Like Receptor 3-Mediated Immune Response in Herpes Simplex Encephalitis |
| title_full_unstemmed | Corilagin Interferes With Toll-Like Receptor 3-Mediated Immune Response in Herpes Simplex Encephalitis |
| title_short | Corilagin Interferes With Toll-Like Receptor 3-Mediated Immune Response in Herpes Simplex Encephalitis |
| title_sort | corilagin interferes with toll like receptor 3 mediated immune response in herpes simplex encephalitis |
| topic | corilagin herpes simplex virus type 1 inflammation signaling pathway toll-like receptor 3 |
| url | https://www.frontiersin.org/article/10.3389/fnmol.2019.00083/full |
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