Scientists have revealed a new mechanism for salmonella immune escape

recently, Cell-Communication published online the latest results of Yangzhou University Professor Jia Xin'an's team. The team studied the molecular mechanism of salmonella TcpS to play an anti-inflammatory function by interfering with the TLR-NF-B signal path, revealed a new strategy of salmonella immune escape, and provided a new idea for the design of new anti-inflammatory small molecule drugs by evaluating the anti-inflammatory effect of the functional peptide segment of TcpS in the over-inflammatory reaction.
salmonella is an important type of zoonotic disease progenitor bacteria, which is harmful to livestock and poultry breeding industry and causes public health problems. Therefore, the study of salmonella infection and immune mechanism is of great significance.
team identified genetic tcpS containing Coiled-coil and TIR domains in salmonella and determined that enteritis salmonella secretes TcpS proteins through T3SS1. TcpS evades the natural immune response by simulating the TIR domain of TLRs to interfere with the TLR-NF-B signaling path, inhibiting the nucleation of p65 and the secretion of inflammatory cytokines.
salmonella inhibits inflammatory response in the early stages of infection, promotes its proliferation in the body, and eventually causes inflammatory storms in the blood later in infection, resulting in tissue pathological damage. The study further determined that TIR-TcpS peptides inhibited the production of inflammatory factors induced by LPS, the activity of p-ERK and p-JNK, and reduced the inflammatory response and release of hemoglobin in mouse serum, while SR4 polypeptides had a good protective effect on mice in the H1N1 influenza virus attack model. By identifying key functional peptide segments in the TcpS protein, it can be used as a reference for the development of potential therapeutic drugs for over-inflammatory reactions or autoimmune diseases. (Source: Li Chen, China Science Journal)
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