Zinc Supplementation Modulates NETs Release and Neutrophils' Degranulation

Area of Science:

• Immunology
• Nutritional Biochemistry

Background:

• Zinc is an essential microelement crucial for the immune system and innate immunity responses.
• Neutrophils are key players in innate immunity, and their functions are influenced by zinc levels.
• Previous research on zinc's role in neutrophil function is fragmentary, necessitating comprehensive investigation.

Purpose of the Study:

• To comprehensively assess the impact of zinc on fundamental neutrophil functions.
• To investigate the effects of zinc on human and murine neutrophils in vitro.
• To examine the in vivo effects of zinc deficiency and supplementation on neutrophil function using a murine model.

Main Methods:

• In vitro incubation of human and murine neutrophils with zinc.
• Analysis of neutrophil phagocytosis, oxidative burst, degranulation, and neutrophil extracellular trap (NETs) release.
• Establishment of a murine model for zinc deficiency and zinc supplementation studies.

Main Results:

• Zinc was found to inhibit NETs release and degranulation in both human and murine neutrophils.
• Zinc's inhibition of NETs release is linked to the suppression of histone H3 citrullination.
• Zinc-deficient mice exhibited increased NETs release and enhanced neutrophil degranulation.

Conclusions:

• Zinc significantly modulates neutrophil functions both in vitro and in vivo.
• Maintaining proper zinc levels is essential for the efficient functioning of the innate immune response.
• Zinc's role in regulating neutrophil extracellular traps and degranulation highlights its importance in immune homeostasis.