Neutrophil extracellular traps: new aspects
Н. В. Воробьева
Abstract
Neutrophils are the first line of defense against invading pathogens in the focus of inflammation, where they use effector functions such as phagocytosis, degranulation and formation of reactive oxygen species (ROS). In 2004, Arturo Zychlinsky described an additional neutrophil effector function – the release of neutrophil extracellular traps or NETs. NETs consist of the modified chromatin “decorated” with bactericidal proteins from granules, nucleus, and cytoplasm. The release of NETs can be activated by a variety of physiological and pharmacological stimuli, and depends on the formation of ROS, the main source of which is enzymatic complex NADPH oxidase. In the process of NET formation, bactericidal granule components exit from granules into cytoplasm, the modification of histones leading to chromatin decondensation, the destruction of the nuclear envelope and cytoplasmic membrane, and the extrusion of chromatin outside the cell are taking place. However, the uncontrolled NET release is a provoking factor in the development of various inflammatory and autoimmune diseases. NETs have been discovered at autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, psoriasis, and vasculitis; NETs are involved in the pathogenesis of cardiovascular, pulmonary, and oncological diseases. In this review, the basic molecular mechanisms of NETs formation, as well as their role in the physiological processes and pathogenesis of a number of diseases including COVID-19 are discussed.