Fig. 1

Processes of the inflammatory response and resolution. Extra stimulus will cause the injury of resident cells, such as epithelial cells, and cause the inflammation onset (1). These cells will be activated and release soluble pro-inflammatory mediators, which can mediate microvascular change, and promote leukocytes influx (neutrophils or eosinophils) (2). The basic function of leukocytes is to phagocyte and thereby to eliminate microorganisms and tissue debris (3). The resident cells and leukocyte in the inflammation center will produce cytokines to induce macrophage polarization and neutrophils recruit to the inflammation center (4,5). M1 cells will transform to M2 with the pro-resolution mediator to attend to the resolution phase (6). Neutrophil apoptosis (7) followed by efferocytosis (6,8) clear dysfunctional cells from the tissue. After clear the phagocytes, pro-resolving will promote macrophage program apoptosis. Excessive macrophage or non-apoptotic macrophage will leave the inflammatory site (9) or/and migrate to the lymphatic (10a,10b). At the end of inflammation resolution, resident immune cells regaining to form “adaptive immune” (11), which creates a status of “post-resolution”