CD11b is involved in coxsackievirus B3-induced viral myocarditis in mice by inducing Th17 cells
Autor: | Sheng-Jian Lu, Shuai Yuan, Heng Wei, Yu-Xin Wen, Yan-Li Liu, Chong-Kai Lin |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
Pathology
medicine.medical_specialty Viral Myocarditis Myocarditis QH301-705.5 Spleen th17 cells General Biochemistry Genetics and Molecular Biology Pathogenesis Immune system medicine cd11b Cytotoxic T cell coxsackievirus b3 Biology (General) General Immunology and Microbiology biology General Neuroscience medicine.disease viral myocarditis medicine.anatomical_structure Integrin alpha M biology.protein Immunohistochemistry General Agricultural and Biological Sciences Research Article |
Zdroj: | Open Life Sciences, Vol 15, Iss 1, Pp 1024-1032 (2020) Open Life Sciences |
ISSN: | 2391-5412 |
Popis: | Viral myocarditis (VMC) caused by coxsackievirus B3 (CVB3) infection is a life-threatening disease. The cardiac damage during VMC is not mainly due to the direct cytotoxic effect of the virus on cardiomyocytes but mostly involves the induction of immune responses. Integrin CD11b plays an important role in immune response, for instance, in the induction of Th17 cells. However, the role of CD11b in the pathogenesis of VMC remains largely unknown. In the present study, a mouse model of VMC was established by CVB3 infection and CD11b was knocked down in the VMC mice by transfection with siRNA-CD11b. The expression of CD11b and IL-17 in heart tissues, frequency of Th17 cells in spleen tissues and serum IL-17 levels were measured using quantitative RT-PCR, Western blot, immunohistochemistry, flow cytometry and ELISA. Results showed that CVB3 infection caused the pathological changes in heart tissues with the increases in the following indexes: expression of CD11b and IL-17 in heart tissues, frequency of Th17 cells in spleen tissues and serum IL-17 levels. The expression of CD11b was positively correlated with IL-17 expression in heart tissues. Depletion of CD11b attenuated the damage caused by CVB3 and decreased the frequency of Th17 cells in spleen tissues as well as in IL-17, IL-23 and STAT3 expression in heart tissues. In summary, our findings reveal that disruption of CD11b function reduced CVB3-induced myocarditis, suggesting that CD11b may be a novel therapeutic target for VMC. |
Databáze: | OpenAIRE |
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