A growing number of studies have demonstrated the importance of
ATP(e)-signalling via P2 receptors as an important component of the inflammatory response to
infection. More recent studies have shown that
ATP(e) can also have a direct effect on
infection by intracellular pathogens, by modulating membrane trafficking in cells that contain vacuoles that harbour intracellular pathogens, such as mycobacteria and chlamydiae. A conserved mechanism appears to be involved in controlling
infection by both of these pathogens, as a role for
phospholipase D in inducing fusion between lysosomes and the vacuoles has been demonstrated. Other P2-dependent mechanisms are most likely operative in the cases of pathogens, such as Leishmania, which survive in an acidic phagolysosomal-like compartment.
ATP(e) may function as a "danger signal" that alerts the immune system to the presence of intracellular pathogens that damage the host cell, while different intracellular pathogens have evolved
enzymes or other mechanisms to inhibit
ATP(e)-mediated signalling, which should, thus, be viewed as
virulence factors for these pathogens.