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MyD88 innate immune function in a zebrafish embryo infection model.


ABSTRACT: 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.

SUBMITTER: van der Sar AM 

PROVIDER: S-EPMC1418923 | biostudies-literature | 2006 Apr

REPOSITORIES: biostudies-literature

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MyD88 innate immune function in a zebrafish embryo infection model.

van der Sar Astrid M AM   Stockhammer Oliver W OW   van der Laan Carina C   Spaink Herman P HP   Bitter Wilbert W   Meijer Annemarie H AH  

Infection and immunity 20060401 4


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 sig  ...[more]

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