Fig. 1

Effects of the neutrophil (PMN) proteins CAP37, neutrophil elastase, and cathepsin G on inflammation and host defense. a CAP37 released from secretory or azurophil granules of PMN can accumulate on proteoglycans on endothelial cells. CAP37 on proteoglycans activates monocytes by increasing intracellular calcium mobilization which leads to increased monocyte adhesion to endothelial cells. b CAP37 and cathepsin G released from neutrophils within the injured/infected tissues are chemotactic for monocytes, causing more monocytes to extravasate into the tissue. c CAP37 increases the expression of adhesion proteins (ICAM-1, VCAM-1, PECAM-1) on endothelial cells, leading to the attachment and extravasation of more monocytes and PMNs into the tissue. d Secreted neutrophil elastase and cathepsin G cleave various cytokines and chemokines leading to their activation (green) or inactivation (red). Neutrophil elastase cleaves progranulin, an anti-inflammatory protein, and prevents its anti-inflammatory functions. Neutrophil elastase also cleaves and inactivates the chemokine SDF-1α. Both neutrophil elastase and cathepsin G cleave and inactivate the pro-inflammatory cytokines TNF-α and IL-6. Cathepsin G cleaves and activates the chemokines CXCL5 and CCL15 leading to recruitment of more immune cells