Model of MMPs orchestrating the pro- and anti-inflammatory response. In response to host challenge, MMPs are released from epithelial cells, resident macrophages, and neutrophils cleaving and activating specific chemokines that recruit PMNs (mCXCL5, hCXCL5, and hCXCL8). After 24-48 hours, macrophages accumulate at the site of injury and secrete MMP-12 that inactivates ELR⁺ CXC chemokines. Hence, in addition to apoptosis reducing the numbers of cells from the PMN influx, by blocking the continued recruitment of PMNs, macrophage MMP-12 contributes to the reduction in the number of PMNs at the site of stimulus. In addition, MMP-12 and other MMPs released from surrounding stromal fibroblasts or epithelial cells cleave and inactivate MCPs (CCL2, -7, -8, and -13) converting these to receptor antagonists disrupting the recruitment of further macrophages and contributing to inflammatory resolution. Hence, macrophages terminate the PMN and macrophage influxes.