Pathogenic Roles of Macrophage Migration Inhibitory Factor during Dengue Virus Infection
Dengue virus (DENV) infection is the most common cause of viral hemorrhagic fever, which can lead to life-threatening dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS). Hemorrhage and plasma leakage are two major hallmarks of DHF/DSS. Because the mechanisms causing these pathogenic changes ar...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2015/547094 |
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| author | Yung-Chun Chuang Hong-Ru Chen Trai-Ming Yeh |
| author_facet | Yung-Chun Chuang Hong-Ru Chen Trai-Ming Yeh |
| author_sort | Yung-Chun Chuang |
| collection | DOAJ |
| description | Dengue virus (DENV) infection is the most common cause of viral hemorrhagic fever, which can lead to life-threatening dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS). Hemorrhage and plasma leakage are two major hallmarks of DHF/DSS. Because the mechanisms causing these pathogenic changes are unclear, there is no effective therapy against DHF/DSS. In this review, we focus on the possible pathogenic effects of a pleiotropic cytokine, macrophage migration inhibitory factor (MIF), on the pathogenesis of DENV infection. MIF is a critical mediator of the host immune response and inflammation, and there is a correlation between the serum levels of MIF and disease severity in dengue patients. Furthermore, MIF knock-out mice exhibit less severe clinical disease and lethality. However, the role of MIF in the pathogenesis of DHF/DSS is not limited to immune cell recruitment. Recent evidence indicates that DENV infection induced MIF production and may contribute to vascular hyperpermeability and viral replication during DENV infection. The expression of both adhesion and coagulation molecules on MIF-stimulated monocytes and endothelial cells is also increased, which may contribute to inflammatory and anticoagulatory states during DHF/DSS. Therefore, blocking MIF production or its function may provide a solution for the treatment and prevention of DHF/DSS. |
| format | Article |
| id | doaj-art-6bc486dc5b2f4223968a329d686b8e06 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-6bc486dc5b2f4223968a329d686b8e062025-02-03T05:51:44ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/547094547094Pathogenic Roles of Macrophage Migration Inhibitory Factor during Dengue Virus InfectionYung-Chun Chuang0Hong-Ru Chen1Trai-Ming Yeh2Department of Medical Laboratory Science and Biotechnology, Medical College, National Cheng Kung University, Tainan 70101, TaiwanCenter of Infectious Disease and Signaling Research, Medical College, National Cheng Kung University, Tainan 70101, TaiwanDepartment of Medical Laboratory Science and Biotechnology, Medical College, National Cheng Kung University, Tainan 70101, TaiwanDengue virus (DENV) infection is the most common cause of viral hemorrhagic fever, which can lead to life-threatening dengue hemorrhagic fever/dengue shock syndrome (DHF/DSS). Hemorrhage and plasma leakage are two major hallmarks of DHF/DSS. Because the mechanisms causing these pathogenic changes are unclear, there is no effective therapy against DHF/DSS. In this review, we focus on the possible pathogenic effects of a pleiotropic cytokine, macrophage migration inhibitory factor (MIF), on the pathogenesis of DENV infection. MIF is a critical mediator of the host immune response and inflammation, and there is a correlation between the serum levels of MIF and disease severity in dengue patients. Furthermore, MIF knock-out mice exhibit less severe clinical disease and lethality. However, the role of MIF in the pathogenesis of DHF/DSS is not limited to immune cell recruitment. Recent evidence indicates that DENV infection induced MIF production and may contribute to vascular hyperpermeability and viral replication during DENV infection. The expression of both adhesion and coagulation molecules on MIF-stimulated monocytes and endothelial cells is also increased, which may contribute to inflammatory and anticoagulatory states during DHF/DSS. Therefore, blocking MIF production or its function may provide a solution for the treatment and prevention of DHF/DSS.http://dx.doi.org/10.1155/2015/547094 |
| spellingShingle | Yung-Chun Chuang Hong-Ru Chen Trai-Ming Yeh Pathogenic Roles of Macrophage Migration Inhibitory Factor during Dengue Virus Infection Mediators of Inflammation |
| title | Pathogenic Roles of Macrophage Migration Inhibitory Factor during Dengue Virus Infection |
| title_full | Pathogenic Roles of Macrophage Migration Inhibitory Factor during Dengue Virus Infection |
| title_fullStr | Pathogenic Roles of Macrophage Migration Inhibitory Factor during Dengue Virus Infection |
| title_full_unstemmed | Pathogenic Roles of Macrophage Migration Inhibitory Factor during Dengue Virus Infection |
| title_short | Pathogenic Roles of Macrophage Migration Inhibitory Factor during Dengue Virus Infection |
| title_sort | pathogenic roles of macrophage migration inhibitory factor during dengue virus infection |
| url | http://dx.doi.org/10.1155/2015/547094 |
| work_keys_str_mv | AT yungchunchuang pathogenicrolesofmacrophagemigrationinhibitoryfactorduringdenguevirusinfection AT hongruchen pathogenicrolesofmacrophagemigrationinhibitoryfactorduringdenguevirusinfection AT traimingyeh pathogenicrolesofmacrophagemigrationinhibitoryfactorduringdenguevirusinfection |