**2.3 Intramacrophage survival and replication**

Similar mechanisms occur inside epithelial cells after intestinal invasion and once bacteria have been internalized by macrophages. Briefly, *Salmonella* cells are localized in the SCV once engulfment is completed. Preserving the SCV membrane integrity plays a crucial role in allowing *Salmonella* replication inside these intracellular niches. These procedures are regulated by T3SS-2 transporting action and its translocon machinery, namely SseBCD complex [77]. Hence, the required effectors which are encoded both inside and outside SPI-2 facilitate the success of *Salmonella* intramacrophage survival. The SPI-2 gene expression is triggered in response to a number of environmental signals mimicking the vacuolar environment of SCV, including stationary growth phase, low osmolarity [102], low concentrations of Mg2+, Ca2+ or PO3 [103, 104], and low pH [76]. The expression of SPI-2 genes is coordinately regulated at both transcriptional and post-transcriptional levels. During the transcription of SPI-2 genes, many two-component regulatory systems are involved, including SsrA-SsrB, OmpR-EnvZ and PhoP-PhoQ as well as transcriptional regulators, namely SlyA and the alternative sigma factor of RNA polymerase RpoE. The main regulatory proteins that act post-transcriptionally are the RNA chaperons, including Hfq, CsrA, and SmpB. The *mgtC* gene located in SPI-3 has been shown to contribute to replication in macrophages. All the mentioned virulence determinants can be found in **Table 3** and **Figure 1**.
