Control of myeloid cell trafficking in resolution

Abstract

Following tissue injury or microbial invasion, neutrophils are robustly recruited to inflammatory loci, which is a hallmark of the host inflammatory response. This event initiates a series of processes required to activate resolution, including recruitment of monocytes, clearance of microbes, cellular debris and apoptotic neutrophils, the egress of phagocytes and, ultimately, regain of tissue homeostasis. Substantial evidence now signifies that resolution of inflammation is a highly coordinated, active process dictated by the spatial-temporal generation of proresolving mediators that act on specific receptors to modulate cell and tissue reactivity. This review will focus on the mediators, targets and pathways initiated to orchestrate resolution. Importantly, disruption of the key processes involved in inflammatory resolution could result in delayed restoration of tissue homeostasis, leading to fibrosis and/or persistent inflammation.