Figure 6. A model for the role of ATP in facilitating the host defense against bacterial infection.

During bacterial infection, ATP was released by both the infected cells and the bacteria. The released ATP is able to facilitate neutrophil recruitment to the site of infection by three potential mechanisms: (1) directly enhancing neutrophil chemotaxis; (2) inducing chemokine secretion from resident macrophages through the activation of P2Y receptors; (3) inducing NLRP3 inflammasome activation and Interleukin-1β secretion through the P2X7 receptor, while Interleukin-1β further enhances chemokine secretion. The early recruitment of neutrophils facilitated the clearance of bacteria and the survival rate in mice.