Fig. 1.

Galectins may contribute to the spatial and temporal regulation of neutrophil turnover. Intracellular galectin remains reduced and active. However, following cellular injury, intracellular galectin becomes exposed to the extracellular oxidizing environment, oxidizes and becomes inactive. Following galectin inactivation, neutrophils infiltrate, which allows for neutralization of potential pathogens and removal of necrotic tissue. During this inflammatory episode, most of the galectin released during the primary injury likely becomes oxidized, preventing galectins from inhibiting a productive inflammatory response. Following removal of necrotic tissue and removal of pathogens, encroachment of neutrophils on surrounding viable tissue results in cellular damage and release of reduced and therefore active galectin. Galectin engages neutrophil receptors and induces PS exposure without altering cellular viability, a process termed preaparesis, which allows neutrophils to maintain membrane integrity until successfully phagocytosed