Wangshu Xu1,2, Heng Zhou1,2, Xiaojuan Li3, Lu Wang4, Xinwu Guo5, Linlin Yin1,2, Haoxiao Chang1,2, Yuzhen Wei1,2, Qingsong Li6, Jinhai Deng4, Xingang Zhou7, Haifeng Yang8, Xinghu Zhang1,2, Fang Yi9, Wenping Ma10. 1. Department of Neurology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, China. 2. China National Clinical Research Center for Neurological Diseases, Beijing 100050, China. 3. Department of Radiology, The First Hospital of Harbin Medical University, Harbin 150001, China. 4. Department of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China. 5. Sansure Biotech Inc., Changsha 410205, China. 6. Department of Laboratory Medicine, Peking University Third Hospital, Beijing 100191, China. 7. Department of Pathology, Beijing Ditan Hospital, Capital Medical University, Beijing 100015, China. 8. Department of Neurosurgery, Xuanwu Hospital, Capital Medical University, Beijing 100053, China. 9. Department of Neurology Lishilu Outpatient, PLA Rocket Force General Hospital, Beijing 100045, China. 10. Department of Medical Genetics, School of Basic Medical Sciences, Peking University Health Science Center, Beijing 100191, China.
Abstract
BACKGROUND: Herpes simplex encephalitis (HSE), an acute inflammatory disease of the central nervous system is caused by the herpes simplex virus infection. HSE occurs at any age, and it is often accompanied by high mortality and neurological dysfunction. The C1Q/TNF-related protein (CTRP) family, usually contains a homotrimeric structure, which comprises the N-terminal signal peptide and the C-terminal C1q globular domain. It has been demonstrated that CTRPs play pivotal roles in the inflammation process. CTRP4 is a member of the CTRP family and contains two C1q globular domains. Moreover, evidence shows that the recombinant human CTRP4 (rhCTRP4) protein exerts satisfactory anti-inflammatory effects in experimental colitis models via the NF-κB pathway. However, its role in inflammation-related neurological diseases remains unknown. METHODS: The purpose of this study is to evaluate the expression of CTRP4 and its correlation with HSE progression. We determined the serum CTRP4 levels in a normal brain, tuberculous meningitis (TBM), bacterial meningitis (BM) and HSE. RESULTS: We found that compared to a normal brain, TBM and BM, CTRP4 was significantly increased in HSE. Moreover, in the course of HSE, serum interleukin (IL-6) and necrosis factor-α (TNF-α) were also increased and were closely associated with CTRP4 expression. CTRP4 expression was examined by immunohistochemistry (IHC) in the normal control brain tissues, HSE, TBM and BM brain tissues. High positively expression of CTRP4 was found in HSE. In the normal brain tissue, TBM, and BM brain tissues, CTRP4 showed a weak expression. In the clinical evaluation, CTRP4 expression correlated closely with an ascending stage of the disease [mini-mental state examination (MMSE) evaluation, MRI imaging). CONCLUSIONS: Our findings suggest that CTRP4 is highly expressed in HSE and is closely related to the progression of HSE. Thus, CTRP4 may serve as a potential severity index for HSE and targeting CTRP4 might be a promising therapeutic strategy against HSE.
BACKGROUND: Herpes simplex encephalitis (HSE), an acute inflammatory disease of the central nervous system is caused by the herpes simplex virus infection. HSE occurs at any age, and it is often accompanied by high mortality and neurological dysfunction. The C1Q/TNF-related protein (CTRP) family, usually contains a homotrimeric structure, which comprises the N-terminal signal peptide and the C-terminal C1q globular domain. It has been demonstrated that CTRPs play pivotal roles in the inflammation process. CTRP4 is a member of the CTRP family and contains two C1q globular domains. Moreover, evidence shows that the recombinant human CTRP4 (rhCTRP4) protein exerts satisfactory anti-inflammatory effects in experimental colitis models via the NF-κB pathway. However, its role in inflammation-related neurological diseases remains unknown. METHODS: The purpose of this study is to evaluate the expression of CTRP4 and its correlation with HSE progression. We determined the serum CTRP4 levels in a normal brain, tuberculous meningitis (TBM), bacterial meningitis (BM) and HSE. RESULTS: We found that compared to a normal brain, TBM and BM, CTRP4 was significantly increased in HSE. Moreover, in the course of HSE, serum interleukin (IL-6) and necrosis factor-α (TNF-α) were also increased and were closely associated with CTRP4 expression. CTRP4 expression was examined by immunohistochemistry (IHC) in the normal control brain tissues, HSE, TBM and BM brain tissues. High positively expression of CTRP4 was found in HSE. In the normal brain tissue, TBM, and BM brain tissues, CTRP4 showed a weak expression. In the clinical evaluation, CTRP4 expression correlated closely with an ascending stage of the disease [mini-mental state examination (MMSE) evaluation, MRI imaging). CONCLUSIONS: Our findings suggest that CTRP4 is highly expressed in HSE and is closely related to the progression of HSE. Thus, CTRP4 may serve as a potential severity index for HSE and targeting CTRP4 might be a promising therapeutic strategy against HSE.
Entities:
Keywords:
C1Q/TNF-related protein 4 (CTRP4); correlation; herpes simplex encephalitis (HSE); mini-mental state examination (MMSE)
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