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In order to phagocytose pathogens, macrophages must activate and activate the actin-based machinery required to form the phagocytic cup, establish contact with the particle, internalize it and digest it. The molecular details of these processes are beginning to be elucidated and the data indicate that phosphoinositide 3-kinase (PI 3-kinase) plays a key role in the regulation of actin dynamics in this type of cell. In particular, PI 3-kinase is regulated in response to microbial products and can activate the Rac, an activator of actin polymerization, in a variety of cell types. The data also indicate that in phagocytes, LY294002, a specific PI 3-kinase inhibitor, does not prevent phagocytosis but blocks the recruitment of the Arp2/3 complex to the phagocytic cup and the enrichment of some actin regulators at the site of phagocytosis. In addition, in LY294002-treated phagocytes, the response of other actin regulators, such as cortactin, is inhibited. The data indicate that PI 3-kinase is not a primary negative regulator of actin dynamics in phagocytes. Nonetheless, as phagocytosis of pathogenic particles is a key effector function of macrophages, an understanding of the molecular aspects of this process might ultimately provide information of value in the search for therapeutic agents.Q:

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