Neutrophils are the first leukocyte recruited from the blood stream to the injured tissue. It is thought that neutrophils die at the site of infection; however several studies have suggested that this may not be the case. Using photoconvertible mice, we have investigated neutrophil egress from sites of inflammation. Following microbial, but not sterile injury, neutrophils migrate from the skin to the draining lymph node. Moreover they comprise 80% of the cells migrating from the skin to the draining lymph node early after infection. Intravital microscopy and antibody blocking experiments have shown that neutrophil egress occurs via the lymphatics and is CD11b dependent.
We have also investigated the role of neutrophils in the adaptive immune response. Eight hours following S. aureus infection neutrophils contain antigen, express MHC-II and the co-stimulatory molecules CD80 and CD86. Furthermore neutrophil depletion augments lymphocyte proliferation in the early adaptive immune response. All together these data challenge the dogma that neutrophils die at the site of inflammation, identify a mechanism for neutrophil egress from inflamed tissue and suggest that neutrophils may mediate initial communication between the site of injury and the adaptive immune system.