Figure 5.

Galectin regulation of neutrophil turnover. As the intracellular environment is reducing, intracellular stores of galectin remain active. However, following cellular injury, intracellular galectin becomes exposed to the extracellular oxidizing environment, where galectin oxidation and inactivation may occur. Rapid infiltration of neutrophils following injury allows for neutralization of potential pathogens and removal of necrotic tissue. As most extracellular galectin may become oxidized following injury prior to significant neutrophil recruitment, the ability of galectins to induce neutrophil turnover would be compromised, preventing galectins from inhibiting a productive inflammatory response. Following removal of necrotic tissue and pathogens, neutrophil encroachment on surrounding viable tissue results in cellular damage and release of reduced and therefore active galectin. Released galectins then engage neutrophils impinging on surrounding viable tissue, induce an oxidative burst that facilitates killing of ingested pathogens and the induction of PS exposure. As galectin-induced PS exposure occurs in the absence of apoptosis, this allows neutrophils to maintain membrane integrity in an otherwise inflammatory environment until successfully phagocytosed by monocyte-differentiated macrophages, which are typically outnumbered by neutrophils and are recruited after significant neutrophil influx. Once neutrophils are removed and inflammation subsides, tissue repair and regeneration ensue.