Project description:Edwardsiella tarda is a Gram-negative bacterial pathogen that can infect a wide range of freshwater and marine fish. However, the immune evasion mechanisms of Edwardsiella tarda is not fully understood. We found that Edwardsiella tarda infection generally significantly upregulated and downregulated a lot of immune-related genes of zebrafish ZF4 cells using RNA-seq technology.
Project description:This SuperSeries is composed of the following subset Series: GSE28481: Transcriptome analysis of the zebrafish embryonic host response to Edwardsiella tarda infection using a static immersion systems [experiment A] GSE28485: Transcriptome analysis of the zebrafish embryonic host response to Edwardsiella tarda infection [experiment B] Refer to individual Series
Project description:Transcriptome analysis of the zebrafish embryonic host response to Edwardsiella tarda infection using a static immersion systems [experiment A]
Project description:Gene expression profiles by microarray have contributed for a elucidation of an immune-response and a determination of efficiency in vaccination. Recent day, edwardsielosis have caused a fatal damage in the aquaculture of Japanese flounder, Paralichthys olivaceus. However the formalin killed-cell vaccines made from Edwardsiella tarda isolated same fish species were not efficient. Recent our study revealed the mixed FKC vaccine made from the two different type of E. tarda protected Japanese flounder against Edwardsiella tarda infection for long-term. In this study, we analyzed the immune-response of a vaccinated fish kidney using the mixed FKC vaccine against Edwardsiella tarda with an Agilent custom-oligo DNA microarray on 9,573 probes of Japanese flounder. Our study revealed that the mixed FKC vaccine confered a strong immune-response and keeped a efficient for long-term on Japanese flounder.
Project description:Transcriptional profiling of the zebrafish embryonic host response to infection by injection of 200 CFUs of Edwardsiella tarda (strain FL6-60)
Project description:Transcriptional profiling of the zebrafish embryonic host response to infection by injection of 200 CFUs of Edwardsiella tarda (strain FL6-60) All infection experiments were performed using mixed egg clutches of Albino strain zebrafish. Embryos were staged at 28 hours post fertilization (hpf) by morphological criteria and approximately 200 cfu of mCherry expressing E. tarda bacteria were injected into the caudal vein close to the urogenital opening. As a control an equal volume of PBS was likewise injected. Single embryos of the infected and control group were collected 8 hours post infection (hpi).
Project description:MyD88 is an adaptor protein in Toll-like receptor and interleukin 1 receptor mediated signaling pathways that plays an essential role in activation of immune responses following pathogen recognition. We investigate that role in the zebrafish embryo model by using a zebrafish mutant line that contains a premature stop condon in the gene encoding MyD88, leading to a truncated protein that lacks domains important for its normal function. We infected these MyD88 mutants and wildtype individuals with Salmonella typhimurium and Edwardsiella tarda to compare the resulting immune response by transcriptome profiling on total RNA isolated from single embryos. The data derived from these microarray experiments confirms the vital role of MyD88 in pathogen recognition and provides many leads for further research. This microarray study was designed to determine the effect of a truncation of the MyD88 protein on the innate immune response of zebrafish embryos during infection with Salmonella typhimurium and Edwardsiella tarda. Embryos used in this study are derived from an incross between parents heterozygous for the mutation. Both homozygous mutants and their wildtype siblings were selected by genotyping after being injected with the bacteria or PBS as control. RNA was isolated from single embryos and each treatment group consisted of three embryos: (1) Homozygous mutants injected with PBS 8 hours post infection (hpi), (2) wildtype siblings injected with PBS 8hpi, (3) S. typhimurium-infected homozygous mutants 8hpi, (4) S. typhimurium-infected wildtype siblings 8hpi, (5) Homozygous mutants injected with PBS 8 hours post infection (hpi) (E.tarda control), (6) wildtype siblings injected with PBS 8hpi (E. tarda control), (7) E. tarda-infected homozygous mutants 8hpi, (8) E. tarda-infected wildtype siblings 8hpi. Embryos were grown at 28.5M-bM-^@M-^S30M-BM-0C in egg water and manually dechorionated at 24 hours post fertilization (hpf). Subsequently, embryos were infected at 28 hpf by micro-injecting 200 colony forming units (CFU) of S. typhimurium SL1027 or E. Tarda FL-F60, or were mock-injected with buffer as a control. After injections embryos were transferred into fresh egg water and incubated for 8 h or 4 days at 28M-BM-0C. After the incubation period, single embryos were snap-frozen in liquid nitrogen and RNA was isolated for microarray analysis. All treatment groups were analyzed using a common reference approach.