A Comparative Analysis of <i>Edwardsiella tarda</i>-Induced Transcriptome Profiles in RAW264.7 Cells Reveals New Insights into the Strategy of Bacterial Immune Evasion

• Main Authors: Huili Li, Boguang Sun, Xianhui Ning, Shuai Jiang, Li Sun
• Format: Article
• Language: English
• Published: MDPI AG 2019-11-01
• Series: International Journal of Molecular Sciences
• Subjects: <i>edwardsiella tarda</i>; macrophage; infection; transcriptome; immune evasion
• Online Access: https://www.mdpi.com/1422-0067/20/22/5724

<i>Edwardsiella tarda</i> is a Gram-negative bacterial pathogen with a broad host range, including fish, reptiles, and mammals. One prominent virulence feature of <i>E. tarda</i> is its ability to survive and replicate in host phagocytes, but the relevant molecular mechanism is largely unknown. In this study, we examined the transcriptome profiles of RAW264.7 cells, a murine macrophage cell line, infected with live <i>E. tarda</i> or stimulated with dead <i>E. tarda</i> for 4 h and 8 h. Eighteen libraries were constructed, and an average of 69 million clean reads per library were obtained, with ~81.63% of the reads being successfully mapped to the reference genome. In total, 208 and 232 differentially expressed genes (DEGs) were identified between live and dead <i>E. tarda</i>-treated cells at 4 h and 8 h post-infection, respectively. The DEGs were markedly enriched in the Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways associated with immunity. Live <i>E. tarda</i> differed strikingly from dead <i>E. tarda</i> in the regulation of immune related genes. Compared with dead <i>E. tarda</i>-treated cells, live <i>E. tarda</i>-treated cells exhibited marked and significant suppression in the induction of a large amount of immune genes, including RIG-I-like receptors, cytokines, and interferon-related genes. Furthermore, some of the immune genes highly regulated by live <i>E. tarda</i> formed complicated interaction networks with each other. Together, the results of this study revealed a transcriptome profile specifically induced by the active virulence elements of live <i>E. tarda</i> during the infection process, thus adding new insights into the intracellular infection mechanism of <i>E. tarda</i>. This study also provided a valuable set of target genes for further study of the immune evasion strategy of <i>E. tarda</i>.