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MyD88 Innate Immune Function in a Zebrafish Embryo Infection Model

Innate immunity signaling mechanisms during vertebrate embryogenesis are largely unknown. To study Toll-like receptor (TLR) signaling function in the zebrafish embryo model, we designed an experimental setup for antisense morpholino knockdown under conditions of bacterial infection. Clearance of Sal...

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Bibliographic Details
Published in:Infection and Immunity 2006-04, Vol.74 (4), p.2436-2441
Main Authors: Sar, Astrid M. van der, Stockhammer, Oliver W, Laan, Carina van der, Spaink, Herman P, Bitter, Wilbert, Meijer, Annemarie H
Format: Article
Language:English
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Summary:Innate immunity signaling mechanisms during vertebrate embryogenesis are largely unknown. To study Toll-like receptor (TLR) signaling function in the zebrafish embryo model, we designed an experimental setup for antisense morpholino knockdown under conditions of bacterial infection. Clearance of Salmonella enterica serovar Typhimurium Ra bacteria was significantly impaired after knockdown of myeloid differentiation factor 88 (MyD88), a common adaptor protein in TLR and interleukin-1 receptor signaling. Thereby, we demonstrate for the first time that the innate immune response of the developing embryo involves MyD88-dependent signaling, which further establishes the zebrafish embryo as a model for the study of vertebrate innate immunity.
ISSN:0019-9567
1098-5522
DOI:10.1128/IAI.74.4.2436-2441.2006