Salmonella Typhimurium remains a constant concern in breeding by its financial impact: loss of yield, animal death, persistence in farms. In human health, it remains the second most deadly foodborne infectious agent. This facultative intracellular bacterium is able to invade, survive and replicate in a large panel of phagocytic and non-phagocytic cells. Type III secretion system 1 (T3SS-1) and 2 (T3SS-2) are historically described as essential for Salmonella invasion and multiplication. T3SS1 and its effectors are involved in the entry and in several stages of the formation and maintenance of the endocytosis vacuole. T3SS-2 and its effectors are involved in the biogenesis of SCV leading to Salmonella replication. Several study agree that Salmonella with nonfunctional T3SS-1 are able to induce naturally in humans or experimentally in murine and bovine intestinal pathologies. Moreover, two entry factors have recently been described (Rck and PagN). The objective of this study is to define the consequences of absence of functional T3SS-1 on the behavior of Salmonella in a non-phagocytic cell model permissive to the entry of a T3SS-1 deficient Salmonella (invA mutant) at a similar level than the wild type strain. By confocal and electron microscopy we have observed that the wild type strain, did not induce Trigger mechanism despite of T3SS-1 effectors translocation but rather a zipper like mechanism and is able to survive and multiply in a mature vacuole. The Salmonella invA mutant also induce a Zipper like membrane rearrangement and is able to survive and multiply in mature vacuole by a similar process. The observation made with this permissive cell model give an opportunity to decipher the dialogue between bacterial and cell partners allowing bacteria survival usually known to be dependent first of all of T3SS-1 effectors.