Neutrophils play a crucial role in the host’s defense against invading microbes. The release of neutrophil extracellular traps is one of the strategies they utilize to remove infections (NETs). Although the cellular components and factors determining or aiding NET formation have been extensively explored, the cellular components and factors determining or promoting NET formation remain unknown.
For a study, researchers showed that intact F-actin dynamics and myosin II function were required for NET formation when induced by different stimuli, such as phorbol 12-myristate 13-acetate, monosodium urate crystals, and Candida albicans, using various actin polymerization and myosin II modulators on neutrophils from healthy individuals. The absence of reactive oxygen species generation or granule release, which were normal or augmented under the indicated circumstances, could not explain the involvement of actin polymerization in NET formation.
Neutrophils from patients with extremely uncommon hereditary actin polymerization deficiencies caused by either actin-related protein 2/3 complex subunit 1B deficiency or megakaryoblastic leukemia 1 deficiency did not demonstrate NETosis. Instead, they discovered that when actin dynamics were inhibited, there was a lack of translocation of neutrophil elastase to the nucleus, which may explain the defective NET formation. The findings indicated that an intact and active actin polymerization process and active myosin II were required for neutrophils to release nuclear DNA during NET formation.
