Molecular mechanisms underlying Nocardia host interactions

<i>Nocardia</i> species are opportunistic pathogens that cause localized and disseminated infections, particularly in immunocompromised individuals. Despite their clinical importance, the molecular mechanisms underlying <i>Nocardia</i> pathogenicity remain incompletely understood. This review summarizes current advances in <i>Nocardia</i> virulence factors, host immune responses, and intracellular survival strategies. A diverse array of virulence factors enables <i>Nocardia</i> 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 <i>Nocardia</i> 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 <i>Nocardia</i> infection are also briefly summarized. However, most mechanistic studies remain restricted to a limited number of type strains. Further investigations into <i>Nocardia</i>-host interactions are essential for the development of improved diagnostic, therapeutic, and preventive strategies for nocardiosis.