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Dr. Gorvel aims at studying interactions between host cells and pathogenic bacteria such as Salmonella and Brucella. We characterized in vivo the fist target cells in the intestine and the lung after infection with Brucella and Salmonella. In Salmonella he identified the various steps involved in the maturation of the Salmonella-containing vacuole and the establishment of the replication niche are dependent of the expression of several bacterial effector proteins being secreted by the type III secretion system. PipB2, SopD2 and SifA are three Salmonella effector proteins controlling the recruitment of kinesin-1 at the Salmonella-containing vacuole in the presence of the host protein SKIP. PipB2 plays the role of a linker for kinesin and SKIP controls membrane exchanges dependent of kinesin. In Brucella, Dr. Gorvel and his laboratory established that the endoplasmic reticulum is the replication site Brucella in dendritic cells. His efforts have concentrated on the detection of Brucella by the immune system. We have shown that the Brucella LPS plays the role of a shield anti-recognition by the TLR-4/MD2 complex. Also, his laboratory was the first to demonstrate that a new class of bacterial molecules called Btp for Brucella Toll-like interacting proteins, control the signalisation pathway activated by the TLR-agonist interactions. In addition, he has identified a new virulence factor, the beta-cyclic glucan from Brucella and found that, when purified, can be used as an adjuvant.