Modulation of neutrophil recruitment and function is critical for directing inflammatory cells to areas of infection in order to battle invading pathogens while minimizing host tissue harm or autoimmune. Over the years, researchers have been increasingly interested in the underlying processes that regulate the recruitment of neutrophils, one of the most numerous inflammatory cells. The previously reported classical leukocyte recruitment cascade had been expanded to include capture, rolling, adhesion, crawling, and transmigration, as well as a reverse-transmigration stage important for balancing immune defense and controlling distant organ endothelial leakage.
For a study, investigators emphasized the role of cellular interaction, tissue environmental cues, circadian rhythmicity, neutrophil phenotyping detection, differential chemokine sensing, and the involvement of diverse signaling components in receptor activation and integrin conformations. In translational animal models, the utilization of medicines that modulate neutrophil activation responses, as well as mutations that cause defective neutrophil receptors and altered signaling cascades, had been characterized.
Such mutations in humans resulted in greater vulnerability to infections or organ damage. The study focused on recent breakthroughs in the knowledge of the control of neutrophil recruitment and functioning, as well as the translational implications of recent findings in the area, with a particular emphasis on acute inflammation and sepsis.
