In mice, the deliveryof Sal4 IgA via the “backpack tumor” model or by gavageis sufficient to limit bacterial uptake into Peyer’s patchtissues.34,36 It is also reported that Sal4 IgA treatmentinhibits STm motility and abrogates the STm SPI-1 type III secretionsystem (T3SS), each of which contribute to bacterial entry into theepithelial cells.54 The motivation behindour current endeavor was to investigate whether a recombinant humanSIgA form of Sal4 retains biological activity and is able to blockbacterial entry into gut associated-lymphoid tissues when administeredpassively. This evidence concerns the gene SPI1 and neoplasm.