7 From an evolutionary standpoint, it would seem reasonable to conclude that the system has been optimized to allow for bacterial clearance while minimizing surrounding collateral damage. 6ĭuring sterile tissue injuries, neutrophils are also essential to participate in the clearance of cellular debris, returning tissue to homeostasis. 4, 5 This is best exemplified by the fact that neutropenia is the biggest risk factor for infection. 3 Thus, impairment of neutrophil recruitment to an infectious nidus facilitates pathogen dissemination into blood and vital organs, development of systemic infection, and eventual death. 2 Neutrophils display a wide range of effector mechanisms to counteract pathogens that include phagocytosis and the production of reactive oxygen species (ROS), proteases, and neutrophil extracellular traps (NETs). 1 In addition, DAMPs and pathogen-associated molecular patterns may also directly activate receptors on neutrophils to induce recruitment.

During an infection or tissue damage, pathogen-associated molecular patterns and/or damage-associated molecular patterns (DAMPs) are sensed by pattern recognition receptors as well as DAMP receptors, which can activate resident cells to produce inflammatory mediators, such as chemokines CXCL1 and CXCL2, which bind to and activate G-protein–coupled receptors on neutrophils. Neutrophils are the predominant leukocyte population in human blood and among the first cells recruited to an inflammatory site.

Kathy kubes