Molecular mechanisms underlying Nocardia host interactions

Nocardia species are opportunistic pathogens that cause localized and disseminated infections, particularly in immunocompromised individuals. Despite their clinical importance, the molecular mechanisms underlying Nocardia pathogenicity remain incompletely understood. This review summarizes current advances in Nocardia virulence factors, host immune responses, and intracellular survival strategies. A diverse array of virulence factors enables Nocardia to invade host cells, circumvent immune defenses, and maintain persistence within host tissues, including mammalian cell entry (Mce) proteins, antioxidant enzymes, phospholipase C, hemolysins, and siderophore-associated proteins. Host protection against Nocardia relies primarily on innate immune responses, with neutrophils playing a central role and being coordinated by γδT cells and interleukin-17-mediated signaling pathways. In addition, the clinical epidemiology of nocardiosis and animal models of Nocardia infection are also briefly summarized. However, most mechanistic studies remain restricted to a limited number of type strains. Further investigations into Nocardia-host interactions are essential for the development of improved diagnostic, therapeutic, and preventive strategies for nocardiosis.