the neutrophil swarming sites. In the third stage, swarming neutrophils can amplify their recruitment in a feed forward manner through intercellular communication by leukotriene B4 (LTB4). The propagation of neutrophil recruitment leads to multiple, dense neutrophil cell clusters at the site of inflammation. A 2013 study showed that neutrophils lacking the high affinity receptor for LTB4 (LTB4R1) decreased the recruitment of neutrophils at later stages of swarming. In addition, proximal cells to the inflammation site showed chemotaxis similar to the control cells while distant cells were poorly attracted. This finding suggests that the proximal neutrophils that are recruited early on are not affected by the lack of LTB4R1, but distant neutrophils that are required for the propagation of neutrophil swarming are not able to be recruited to the swarming site. These results present LTB4 as a key signaling molecule for a prolonged neutrophil swarm response and recruitment of neutrophils from distant areas of the tissue. Stages 4-5 After stages 1-3, neutrophils slow down in the cell clusters and begin to form aggregates. In this fourth stage, the neutrophil aggregates will aid in rearranging the surrounding extracellular tissue area and create a collagen-free zone at the inflammation center eventually resulting in a wound seal which isolates the site from the rest of the tissue. The exact mechanisms of this are unknown but it is believed that neutrophil proteases from the cell clusters play a role in clearing out the surrounding tissue environment. These neutrophil aggregates become stable as opposed to the constant movement in stages 1-3 by development of high chemoattractant concentrations within the clusters that promote local neutrophil interactions within the cluster. Additionally, neutrophils are switched to an adhesive mode of migration within clusters which further stabilize the aggregates and can prevent neutrophils from leaving the cluster. This switch is believed to be caused by additional secretions of LTB4 and other chemoattractants within the neutrophil aggregates. In stage 5, the swarming response terminates and the clusters dissolve with the resolution of inflammation. Little is known about the mechanisms of this stage but the process may be regulated by neutrophils or external factors from the tissue environment. In a laser-induced skin injury model, neutrophil aggregation typically stopped after 40-60 minutes which occurs at the same time as the appearance of secondary myeloid cell swarms. Knock-in mice studies have shown that the myeloid cells move slower than neutrophils and assemble around the