Abstract
Neutrophils are one of the first cells to arrive at the site of infection, where they apply several strategies to kill pathogens: degranulation, respiratory burst, phagocytosis, and release of neutrophil extracellular traps (NETs). Antibiotics have an immunomodulating effect, and they can influence the properties of numerous immune cells, including neutrophils. The aim of this study was to investigate the effects of azithromycin and chloramphenicol on degranulation, apoptosis, respiratory burst, and the release of NETs by neutrophils. Neutrophils were isolated from healthy donors by density-gradient centrifugation method and incubated for 1 h with the studied antibiotics at different concentrations (0.5, 10 and 50 μg/mL—azithromycin and 10 and 50 μg/mL—chloramphenicol). Next, NET release was induced by a 3 h incubation with 100 nM phorbol 12-myristate 13-acetate (PMA). Amount of extracellular DNA was quantified by fluorometry, and NETs were visualized by immunofluorescent microscopy. Degranulation, apoptosis and respiratory burst were assessed by flow cytometry. We found that pretreatment of neutrophils with azithromycin and chloramphenicol decreases the release of NETs. Moreover, azithromycin showed a concentration-dependent effect on respiratory burst in neutrophils. Chloramphenicol did not affect degranulation, apoptosis nor respiratory burst. It can be concluded that antibiotics modulate the ability of neutrophils to release NETs influencing human innate immunity.
Highlights
Neutrophils are the most abundant immune cells in human peripheral blood, and play a crucial role in the innate immune response by defending the body against pathogens
neutrophil extracellular traps (NETs) are fragile fibers of decondensed chromatin decorated with antimicrobial proteins and histones [1]
These web-like structures are released from the cell to form a physical barrier for the pathogens that limits their spread throughout the organism, and to generate a high local concentration of antimicrobial factors
Summary
Neutrophils are the most abundant immune cells in human peripheral blood, and play a crucial role in the innate immune response by defending the body against pathogens. NETs are fragile fibers of decondensed chromatin decorated with antimicrobial proteins and histones [1] These web-like structures are released from the cell to form a physical barrier for the pathogens that limits their spread throughout the organism, and to generate a high local concentration of antimicrobial factors. Despite their beneficial role, NETs have been reported to contribute to the development of several diseases, including rheumatoid arthritis, diabetes, and thrombosis [2]. A substantial effort is being made to identify agents modulating antimicrobial factors
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