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Neutrophils are a crucial component of the innate immune system, acting as the first line of defense against infection.Their ability to swiftly migrate to sites of infection or injury through a process called chemotaxis is fundamental to their function.This review aims to provide a comprehensive overview of the mechanisms underlying neutrophil chemotaxis, migration, and transmigration.We will explore the signaling pathways, molecular players, and physiological processes that guide neutrophils from the bloodstream to sites of tissue damage or infection.Furthermore, the review will discuss the implications of these processes in disease states and potential therapeutic interventions.Chemotaxis begins with neutrophils detecting chemotactic signals, such as chemokines (e.g., IL-8) and complement components (e.g., C5a), which bind to G-protein-coupled receptors (GPCRs) on their surface.This interaction triggers intracellular signaling cascades involving key molecules like phosphoinositide 3-kinase (PI3K), Akt, and mitogen-activated protein kinases (MAPKs).These pathways regulate cytoskeletal dynamics, enabling neutrophils to move directionally.Actin polymerization at the leading-edge forms pseudopodia, propelling the cell forward, while myosin II-mediated contraction at the rear facilitates coordinated movement.
Maurya et al. (Sat,) studied this question.