Silver Nanoparticles Protect Skin from Ultraviolet B-Induced Damage in Mice

Ho, Yew Kam; Sun, Der-Shan; Chang, Hsin-Hou

doi:10.3390/ijms21197082

Cited by 29 publications

(18 citation statements)

References 44 publications

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“…Wild-type C57BL/6J mice aged 8–12 weeks were purchased from the National Laboratory Animal Center (Taipei, Taiwan) ( 17 , 23 – 27 ). Genetically deficient mice with a C57BL/6J background, including Nlrp3 − / − and Casp1 − / − , were obtained from the Centre National de Recherche Scientifique (Orléans, France) ( 16 , 28 ).…”

Section: Methodsmentioning

confidence: 99%

Exposure of Platelets to Dengue Virus and Envelope Protein Domain III Induces Nlrp3 Inflammasome-Dependent Platelet Cell Death and Thrombocytopenia in Mice

et al. 2021

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In tropical and subtropical regions, mosquito-borne dengue virus (DENV) infections can lead to severe dengue, also known as dengue hemorrhage fever, which causes bleeding, thrombocytopenia, and blood plasma leakage and increases mortality. Although DENV-induced platelet cell death was linked to disease severity, the role of responsible viral factors and the elicitation mechanism of abnormal platelet activation and cell death remain unclear. DENV and virion-surface envelope protein domain III (EIII), a cellular binding moiety of the virus particle, highly increase during the viremia stage. Our previous report suggested that exposure to such viremia EIII levels can lead to cell death of endothelial cells, neutrophils, and megakaryocytes. Here we found that both DENV and EIII could induce abnormal platelet activation and predominantly necrotic cell death pyroptosis. Blockages of EIII-induced platelet signaling using the competitive inhibitor chondroitin sulfate B or selective Nlrp3 inflammasome inhibitors OLT1177 and Z-WHED-FMK markedly ameliorated DENV- and EIII-induced thrombocytopenia, platelet activation, and cell death. These results suggest that EIII could be considered as a virulence factor of DENV, and that Nlrp3 inflammasome is a feasible target for developing therapeutic approaches against dengue-induced platelet defects.

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Section: Methodsmentioning

confidence: 99%

Exposure of Platelets to Dengue Virus and Envelope Protein Domain III Induces Nlrp3 Inflammasome-Dependent Platelet Cell Death and Thrombocytopenia in Mice

et al. 2021

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“…Wild-type C57BL/6J mice aged 8–12 weeks were purchased from the National Laboratory Animal Center (Taipei, Taiwan) ( 14 , 19 – 21 ). Genetically deficient mice with a C57BL/6J background, including Nlrp3 −/− and Casp1 −/− knockout (KO) mice, were obtained from the Centre National de Recherche Scientifique (Orléans, France) ( 10 , 22 ).…”

Section: Methodsmentioning

confidence: 99%

Exposure to Dengue Envelope Protein Domain III Induces Nlrp3 Inflammasome-Dependent Endothelial Dysfunction and Hemorrhage in Mice

Lien

Sun

et al. 2021

Front. Immunol.

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Typically occurring during secondary dengue virus (DENV) infections, dengue hemorrhagic fever (DHF) causes abnormal immune responses, as well as endothelial vascular dysfunction, for which the responsible viral factor remains unclear. During peak viremia, the plasma levels of virion-associated envelope protein domain III (EIII) increases to a point at which cell death is sufficiently induced in megakaryocytes in vitro. Thus, EIII may constitute a virulence factor for endothelial damage. In this study, we examined endothelial cell death induced by treatment with DENV and EIII in vitro. Notably, pyroptosis, the major type of endothelial cell death observed, was attenuated through treatment with Nlrp3 inflammasome inhibitors. EIII injection effectively induced endothelial abnormalities, and sequential injection of EIII and DENV-NS1 autoantibodies induced further vascular damage, liver dysfunction, thrombocytopenia, and hemorrhage, which are typical manifestations in DHF. Under the same treatments, pathophysiological changes in the Nlrp3 inflammasome–deficient mice were notably reduced compared with those in the wild-type mice. These results suggest that the Nlrp3 inflammasome constitutes a potential therapeutic target for treating DENV-induced hemorrhage in DHF.

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“…Wild-type mice of ages 8–12 weeks in C57BL/6J background were purchased from the National Laboratory Animal Center (Taipei, Taiwan) ( 38 , 42 – 46 ). Gene knockout mice with a C57BL/6J background, including Nlrp3 −/− and Casp1 −/− ( 32 ), were obtained from the Center National de Recherche Scientifique (Orléans, France) ( 32 , 33 , 47 ).…”

Section: Methodsmentioning

confidence: 99%

Dengue Virus Envelope Protein Domain III Induces Nlrp3 Inflammasome-Dependent NETosis-Mediated Inflammation in Mice

et al. 2021

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Abnormal immune responses and cytokine storm are involved in the development of severe dengue, a life-threatening disease with high mortality. Dengue virus-induced neutrophil NETosis response is associated with cytokine storm; while the role of viral factors on the elicitation of excessive inflammation mains unclear. Here we found that treatments of dengue virus envelope protein domain III (EIII), cellular binding moiety of virion, is sufficient to induce neutrophil NETosis processes in vitro and in vivo. Challenges of EIII in inflammasome Nlrp3−/− and Casp1−/− mutant mice resulted in less inflammation and NETosis responses, as compared to the wild type controls. Blockages of EIII-neutrophil interaction using cell-binding competitive inhibitor or selective Nlrp3 inflammasome inhibitors OLT1177 and Z-WHED-FMK can suppress EIII-induced NETosis response. These results collectively suggest that Nlrp3 inflammsome is a molecular target for treating dengue-elicited inflammatory pathogenesis.

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Silver Nanoparticles Protect Skin from Ultraviolet B-Induced Damage in Mice

Cited by 29 publications

References 44 publications

Exposure of Platelets to Dengue Virus and Envelope Protein Domain III Induces Nlrp3 Inflammasome-Dependent Platelet Cell Death and Thrombocytopenia in Mice

Exposure of Platelets to Dengue Virus and Envelope Protein Domain III Induces Nlrp3 Inflammasome-Dependent Platelet Cell Death and Thrombocytopenia in Mice

Exposure to Dengue Envelope Protein Domain III Induces Nlrp3 Inflammasome-Dependent Endothelial Dysfunction and Hemorrhage in Mice

Dengue Virus Envelope Protein Domain III Induces Nlrp3 Inflammasome-Dependent NETosis-Mediated Inflammation in Mice

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