The Rab32/BLOC-3-dependent pathway mediates host defense against different pathogens in human macrophages.

ABSTRACT: Macrophages provide a first line of defense against microorganisms, and while some mechanisms to kill pathogens such as the oxidative burst are well described, others are still undefined or unknown. Here, we report that the Rab32 guanosine triphosphatase and its guanine nucleotide exchange factor BLOC-3 (biogenesis of lysosome-related organelles complex-3) are central components of a trafficking pathway that controls both bacterial and fungal intracellular pathogens. This host-defense mechanism is active in both human and murine macrophages and is independent of well-known antimicrobial mechanisms such as the NADPH (reduced form of nicotinamide adenine dinucleotide phosphate)-dependent oxidative burst, production of nitric oxide, and antimicrobial peptides. To survive in human macrophages,

SUBMITTER: Baldassarre M 

PROVIDER: S-EPMC7810368 | biostudies-literature | 2021 Jan

REPOSITORIES: biostudies-literature