Figure 2.

Neutrophil function. PMN extravasation is initiated by inflammatory mediators, which stimulate the upregulation of adhesion molecules, such as selectins, on endothelial cells allowing tethering and rolling of PMN. Chemokine gradients cause PMNs to “crawl” toward the site of infection until an endothelial junction is reached where diapedesis can occur. At the site of infection, neutrophils have numerous functions including phagocytosis, degranulation, and NETosis. Phagocytosis involves the ingestion of a pathogen into a phagolysosome containing granule proteins and ROS, to disable and digest internalized pathogens. Degranulation can also occur extracellularly where granular proteins, such as MPO and elastase, and ROS can be released from PMNs. A novel function of PMNs is NETosis, which is the release of NETs. These decondensed chromatin fibers decorated with histones and granular proteins trap and kill pathogens to prevent further dissemination. It is known that during malaria infection, neutrophils maintain the ability to phagocytose NTS; however, PMNs display impaired ROS production. Mechanisms still to be investigated include: maturation, extravasation, migration, degranulation, and NETosis