ABSTRACT Two mitogen-activated protein kinase (MAPK) modules, ERK 1/2 and p38, are activated by pro-inflammatory stimuli in human neutrophils. The time course and efficacy of MAPK activation depends on the specific stimulus. Chemoattractants and immune complexes stimulate rapid activation, cytokines and LPS stimulate a slow rate of activation, and bacterial phagocytosis stimulates a relatively slow onset of activation. Multiple proximal signal transduction pathways lead to MAPK activation. Both ERK 1/2 and p38 play roles in activation, priming and apoptosis of neutrophils. Defining the molecular mechanisms of MAPK regulation of neturophils responses will provide new targets for pharmacologic manipulation of neutrophil functions.
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