Riboflavin Modulates Complement Activation, Immune Cell Viability and Activation, and Neutrophil Microbicidal...

Riboflavin (vitamin B2) is essential for producing flavin coenzymes (FMN and FAD) involved in redox reactions vital for immune cell functions. However, its direct effects on the immune system, particularly in human neutrophils, have been scarcely studied.

This study examined how physiologically relevant riboflavin concentrations (2.5, 25, and 50 nmol/L) affect complement activation, peripheral blood mononuclear cells (PBMC) viability and activation, and neutrophil functions such as phagocytosis, degranulation, and reactive oxygen species (ROS) production. It used pre-treatment (to simulate prior exposure) and co-treatment (to mimic ongoing supplementation).

Riboflavin affected complement-mediated hemolysis variably depending on treatment. In PBMCs, it improved viability and regulated CD40 expression; in neutrophils, it reduced bacterial phagocytosis dose-dependently during co-treatment, with pre-treatment at 25 nmol/L inhibiting phagocytosis. Riboflavin also decreased extracellular enzyme activity, indicating suppressed degranulation. Intracellular ROS production was dose-dependently reduced during co-treatment; pre-treatment showed a biphasic response, decreasing at 2.5 and 25 nmol/L but increasing at 50 nmol/L.

Riboflavin influences neutrophil functions and immune responses, highlighting the need for further research into its therapeutic potential in conditions characterized by neutrophil hyperactivation.