Some virulence factors of this pathogen are common to other Gram-negative bacteria, which are involved in serious public health issues, and target ancestral mechanisms of the innate immune response preserved in living organisms. This means that host-pathogen interactions can be studied using simple genetic organisms such as the Drosophila fly, thus overcoming the ethical and financial obstacles posed by animal experimentation.

The use of simple genetic organisms, such as the Drosophila fly, to study host-pathogen interactions provides a way of overcoming the ethical and financial obstacles posed by animal experimentation. The importance of the role played by the type III secretion system of the bacteria P. aeruginosa in inducing rapid death in drosophila, and by the ExoS toxin in inhibiting the in vivo cellular immune response has already been demonstrated ^{[1, 2]}. The ExoS toxin GAP domain is able to target all the monomeric GTPases of the Rho family involved in the reorganization of the actin cytoskeleton and, therefore, in cellular chemotaxis at the site of infection and in pathogen phagocytosis. The researcher's latest wirk has revealed that these GTPases are differentially required in the infected organism; in fact, Rac2 plays a key role in resistance to P. aeruginosa. Rac2 is essential for pathogen engulfment by phagocytic cells where it would seem to be the preferred target of the ExoS toxin GAP domain. Conversely, Rac2 is not required to induce Toll and Imd signalling pathways of the innate immune response, which depend on NF-κB factors. The enhanced susceptibility of Rac2-/- flies to bacterial infections illustrates the critical role played by cellular immunity in the control of pathogens ^[3].