Shigella is a bacteria that causes symptoms of dysentery. It affects approximately 165 million people each year globally. It infects host cells using the Type III Secretion System (T3SS). The T3SS is composed of transmembrane proteins that form a needle-like structure, which inserts into the host cell membrane. Once inserted, the T3SS allows effector proteins to be injected into the cytoplasm of the host cell. Invasion plasmid antigen D (IpaD) is a gatekeeper protein that recruits necessary proteins to the tip of the needle when Shigella is near a host membrane. If IpaD is not present, Shigella cannot infect host cells. In order to understand the pathogenesis of Shigella, several mutant strains of IpaD were studied. Hemolytic assays were used to determine the pore-forming capabilities of several IpaD mutants. Strains with the mutations in the N-terminus ranging from amino acid 72 to 77 showed highest hemolytic activity. These were then tested for cytotoxicity, the ability to kill host cells. Further effort will uncover the abilities of these strains. Characterization of IpaD will improve prophylactic and therapeutic treatments for Shigellosis.

Pathogenesis of type III secretion system effector IpaD in Shigella

251st National Meeting (2016)

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