Abstract
Macrophage phagocytosis is critical for defense against pathogens. Whereas many steps of phagocytosis involve ionic flux, the underlying ion channels remain ill-defined. Here, we show that zymosan-, IgG-, and complement-mediated particle binding and phagocytosis are impaired in macrophages lacking the cation channel, Transient Receptor Potential Vanilloid 2 (TRPV2). TRPV2 is recruited to the nascent phagosome and depolarizes the plasma membrane. Depolarization increases phosphatidylinositol-4,5-bisphosphate (PIP2) synthesis, triggering the partial actin depolymerization necessary for occupancy-evoked phagocytic receptor clustering. TRPV2 knockout macrophages are also defective in chemoattractant-evoked motility. Consequently, TRPV2 knockout mice exhibit accelerated mortality and increased organ bacterial load when challenged with Listeria monocytogenes. These data reveal the participation of TRPV2 in early phagocytosis and its fundamental importance in innate immunity.
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