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MOESM4 of Hypoxia and therapeutic treatment of EV-A71 with an immune modulator TLR7 agonist in a new immunocompetent mouse model

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posted on 2019-11-12, 05:03 authored by An-Ting Liou, Chun-Che Liao, Shu-Fan Chou, Ya-Shu Chang, Chih-Shin Chang, Chiaho Shih
Additional file 4: Figure S4. Mouse type Ш IFNs did not protect EV-A71-infected wt-129 mice. a One-week-old wt-129 mice were infected with EV-A71 and treated with three shots of IFNλ (IL28a or IL28b) at different doses on dpi 1, 2 and 3. All mice were monitored daily for survival curve. There was no detectable protective effect from IFNλ treatment. b Genomic DNA was extracted from IL28b genetically modified mice (Materials and Methods), and RT-qPCR was used to distinguish between wild type, heterozygote and homozygote knockout mice. Unlike DNA samples from WT and heterozygote IL-28b (+/−), no PCR signal can be amplified from the DNA sample of the IL28b KO mice. c Unlike the WT B6N mice, IL28b KO mice (lineage clone 1 and clone 2) produced only IFNα (right panel), but no IFNλ (left panel), by poly I:C stimulation. Wild type C57BL/6 N and 3-week-old KO mice were injected with high MW poly I:C via an i.p. route. Sera were collected 4 h post-injection, and both IFNλ and IFNα were measured by the ELISA assay. d One-week-old IL28b KO mice were infected with different genotypes of EV-A71 (gt B5 and C2). Only one out of eleven (1/11) developed paralysis and death. Wild type B6 mice were resistant to EV-A71 infection (0/6). In contrast, the hybrid mice, containing the hSCARB2 receptor transgene and the stat-1 knockout background, were highly susceptible to EV-A71 infection and pathogenesis (10/10).

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