Calcium bursts in neutrophil chemotaxis
Immune cells migrate toward pathogens using chemotactic cues that are either pathogen-derived or generated by the host, such as components of the complement system. During chemotaxis and phagocytosis, the cells coordinate receptor-based signaling with the mechanical processes that underlie adhesion, cell deformation, and migration. To investigate the physiological role of intracellular calcium (Ca2+) bursts in this complex behavior, Francis and Heinrich presented nonadherent human neutrophils with various targets that induced complement-mediated chemotaxis. By simultaneously monitoring the formation of chemotactic pseudopods at the front of the cell and intracellular Ca2+ concentrations, the authors demonstrated that Ca2+ bursts did not accompany the extension of pseudopods and were only induced when the neutrophil contacted the target or was subjected to supraphysiological concentrations of the anaphylatoxin C5a. Thus, Ca2+ bursts, although potentially important for migration on a substrate or phagocytosis, are not required for neutrophils to sense and initiate a response to chemoattractants.
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