SipA, SopA, SopB, SopD, and SopE2 Contribute toSalmonella entericaSerotype Typhimurium Invasion of Epithelial Cells

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Abstract
The centisome 63 type III secretion system (T3SS-1) encoded bySalmonellapathogenicity island 1 (SPI1) mediates invasion of epithelial cells bySalmonella entericaserotype Typhimurium. Characterization of mutants lacking individual genes has revealed that T3SS-1 secreted proteins (effectors) SopE2 and SopB are required for invasion while the SipA protein accelerates entry into cells. Here we have revisited the question of which T3SS-1 effectors contribute to the invasion of epithelial cells by complementing a strain lacking all of the effector genes that are required to cause diarrhea in a calf (asipA sopABDE2mutant). Introduction of either the clonedsipA, the clonedsopB, or the clonedsopE2gene increased the invasiveness of thesipA sopABDE2mutant for nonpolarized HT-29 cells. However, a contribution ofsopAorsopDto invasion was not apparent when invasion assays were performed with the nonpolarized colon carcinoma cell lines T84 and HT-29. In contrast, introduction of either thesopA, thesopB, thesopD, or thesopE2gene increased the invasiveness of thesipA sopABDE2mutant for polarized T84 cells. Furthermore, introduction of a plasmid carryingsipAandsopBincreased the invasiveness of thesipA sopABDE2mutant for polarized T84 cells significantly compared to the introduction of plasmids carrying onlysipAorsopB. We conclude that SipA, SopA, SopB, SopD, and SopE2 contribute toS. entericaserotype Typhimurium invasion of epithelial cells in vitro.