In experimental sepsis, the activation of neutrophils resulted in down-regulation of the expression of their chemokine receptor C-X-C Motif Chemokine Receptor 2 (CXCR2), which impaired the migration of cells to the site of infection, while up-regulation of the receptor expression mediated infiltration of neutrophils in the lungs, kidneys and heart. Here, CXCR2 is linked to infection.