A new mechanism for eduard-host interoperability has been revealed

a new study by Zhang Yuanxing and Liu Qin of the School of Bioengineering of East China University of Technology revealed a new mechanism of bacterial-host interoperability. The results of the research were published online in Public Library of Science - Pathogens.
Eduard's disease is the primary disease that harms the fish farming industry in China, the bacteria is an intracellological parasitic pathogen that secretes a complex molecule called an effect in the course of infection in order to evade or inhibit the host's immune response and improve the ability to colonize and spread pathogens. In-depth analysis of the mechanism between pathogen effects and the host immune system will provide key targets for the vaccine and drug design of Edwardian bacteria.
researchers identified a new sulfur-oxygen-also-protein-effect molecule based on a high-volume screening platform for fish-killing Eduardella effects. Crystal structure analysis found that the protein has conservative -WCxxC-base sequence characteristics, when it is transported to the host cytokine, by simulating endogenetic thiooxygenation protein, target apoptosis signal to regulate the specific spatial binding point of the kinase (ASK1) N, block ask1 phosphorylation, inhibit its downstream Erk/p38-MAPK signal cascading phosphorylation response process.
same time, the researchers built a live model of fish-killing Edwardian microinfills infected zebrafish larvae, further clarifying that activation of the ASK1-MAPK signaling path is one of the key signals for controlling bacterial infections.
this study is the first to discover the role of thioxygen as an effect molecule in bacterial infection, providing a new way of thinking for further analysis of the pathogen-host mutual molecular mechanism. (Source: Huang Xin, China Science Journal)
relevant paper information: