of pathogens, the induction of secondary cell death, and the number of recruited neutrophils. A study that compared large scale tissue damage of sterile mouse tissue by a needle prick with small injuries by a laser beam showed that the needle prick provoked a larger and longer swarm response. After the needle injury, hundreds to thousands of neutrophils were recruited that formed stable cell clusters that sometimes were prolonged for days. In comparison, the neutrophil swarms resulting from the laser induced injury only recruited around 50-330 neutrophils which persisted for a few hours. The presence of pathogens can also increase the size of neutrophil swarms, not necessarily because of their presence as a foreign body, but because of the additional cell death that they can cause in infection sites. When cells are lysed in an infection site, they release an assortment of signaling factors that augment the recruitment of neutrophils to the site. Additionally, neutrophil death during a swarm releases more signaling factors to recruit more neutrophils so the initial amount of neutrophils recruited plays a role in how large the propagation effect is during swarming. Stages Stages 1-3 The neutrophil swarming process is categorized into 5 phases: swarm initiation, swarm amplification, additional swarm amplification through intercellular signaling, swarm aggregation and tissue remodeling, and recruitment of myeloid cells and swarm resolution. The first stage of neutrophil swarming details the “pioneer” neutrophils responding to an infection or inflammation site. The neutrophils close to the injury will switch from random motility to chemotactic movement within a period of 5-15 minutes and swarm towards the infection site. In the second stage, the pioneer neutrophils attract a second wave of neutrophils that come from more distant regions of the tissue. The methods of movement to the region of injury depends on the tissue environment the neutrophils are moving towards. Neutrophil swarming in extravascular spaces such as the connective tissue in the skin involves movement without the assistance of integrin proteins and neutrophil attraction by a gradient of chemoattractants. Neutrophils will be guided by the forces generated by the actomyosin cytoskeleton through the path of least resistance to the site of infection. However, for intravascular tissue environments, neutrophil movement is dependent on integrins and chemoattractant signals on the luminal surface of endothelial cells. In this process, distant neutrophils will be recruited by an inflammatory signal and perform integrin-mediated crawling along the vascular walls to reach