Recent progress in molecular mechanisms of Salmonella effectors involved in gut epithelium invasion

Salmonella enterica is one of the leading infectious pathogens for gastrointestinal illness and affects millions worldwide. Being a foodborne pathogen, Salmonella has developed several molecular strategies to overcome unfavorable conditions in the intestine and to enter and survive in the gut epithelium. This specialized process of host-pathogen interaction is achieved by a series of complex events of adhesion, invasion, and survival. These processes are profoundly regulated by effector proteins encoded in specialized Salmonella pathogenicity islands (SPI). Type-3 Secretion System (T3SS), a molecular assembly of several proteins, is a key for initiating and establishing the interaction of pathogen to host cell. It works as a molecular syringe to deliver effector proteins for a complex invasion process of a pathogen in the host. In this review, we discuss the molecular role of the effector proteins in the invasion of Salmonella pathogen into the gut epithelium of the host. Primarily, effector proteins like SipB and SipC help Salmonella to form translocation assembly and stabilize the host cell structure, allowing bacteria to enter the host cell. Whereas, SopE and SopB further promote membrane ruffling. Next, SptP restores the normal shape of the host cell to ensure the pathogen survives inside the host cell. The pathogen forms a niche, Salmonella-containing vacuoles (SCVs), inside the host cell with the help of SteA, SteC, and PipB2. Further, effectors of the SPI-2 T3SS, including SseB, SseC, and SseD stablize the SCVs and support prolonged bacterial survival. This systematic review provides molecular aspects of these sequential events for the entry of Salmonella into gut epithelium.