Abstract
Polymorphonuclear granulocytes (PMNs; neutrophils) serve as key effector cells in the innate immune system and provide the first line of defense against invading microorganisms. In addition to producing inflammatory cytokines and chemokines and undergoing a respiratory burst that stimulates the release of reactive oxygen species, PMNs also degranulate to release components that kill pathogens. Recently, neutrophil extracellular traps have been shown to be an alternative way to trap microorganisms and contain infection. PMN-derived granule components are also involved in multiple non-infectious inflammatory processes, including the response to myocardial infarction (MI). In this review, we will discuss the biological characteristics, recruitment, activation, and removal of PMNs, as well as the roles of PMN-derived granule proteins in inflammation and innate immunity, focusing on the MI setting when applicable. We also discuss future perspectives that will direct research in PMN biology.
Highlights
Polymorphonuclear granulocytes (PMNs; neutrophils) are a type of leukocyte of approximately 10 μm in diameter that play vital roles in the innate immunity response to pathogens
Persistent neutropenia leads to increased risk of microorganism infections, while excessive recruitment and activation or delayed removal of PMNs results in tissue damage in inflammatory disorders [1]
This review summarizes the roles of PMNs and PMN-derived granule components in inflammation, innate immunity, and myocardial infarction (MI)
Summary
Polymorphonuclear granulocytes (PMNs; neutrophils) are a type of leukocyte of approximately 10 μm in diameter that play vital roles in the innate immunity response to pathogens. PMN microbicidal mechanisms include receptor-mediated phagocytosis and intracellular killing, release of antimicrobial granule contents by degranulation, and the formation of neutrophil extracellular traps (NETs) [9] In addition to their antimicrobial activity, growing evidence suggests that PMNs play an essential role in non-infectious inflammation, innate immunity, and tissue remodeling [10]. In addition to direct antimicrobial activity, lactoferrin inhibits the upregulation of adhesion molecules, limits iron-mediated damage to host tissue, suppresses proinflammatory cytokine production, and limits PMN recruitment [89]. Infiltrating PMNs release a wide range of cytokines and chemokines, granule components, and reactive oxygen species, which directly and indirectly regulate immune cell infiltration and function to modulate remodeling response. The role of NETs in the progression of MI-induced heart failure, has not been investigated
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