Pathogens & immunity · 2026
Mast Cells Control the Bacterial Burden and Grain Formation in Murine Experimental Actinomycetoma Induced by Nocardia brasiliensis.
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Suárez-Vázquez Tomás Alejandro, López-López Nallely, Mejía-Torres Manuel, Rosas-Taraco Adrián G, Garza-Guajardo Raquel, Meneses-Preza Yatsiri G, Ruiz-Sánchez Bibiana Patricia, Chacón-Salinas Rommel, Salinas-Carmona Mario César
Аннотация
BACKGROUND: The immunopathogenesis of actinomycetoma, a chronic granulomatous infection caused primarily by Nocardia brasiliensis, involves poorly defined mechanisms sustaining its characteristic cyclical inflammation.
METHODS: Using MCdeficient KitW-sh/W-sh mice, this study investigated the role of mast cells (MCs) in a murine model of actinomycetoma. Clinical progression, bacterial burden, histopathology, and lesional leukocyte infiltration were analyzed at 30 and 72 days postinfection, and bone marrowderived MCs were challenged in vitro with Nocardia brasiliensis to assess activation.
RESULTS: MC-deficient mice exhibited a significant increase in bacterial load concomitant with attenuated late-phase (72-day) inflammation, characterized by reduced lesional neutrophilia and lymphocytic infiltration. Furthermore, MC absence disrupted the characteristic morphology of bacterial grains. In vitro, N. brasiliensis induced potent MC degranulation and pro-inflammatory cytokine release.
CONCLUSIONS: These data demonstrate that MCs are directly activated by N. brasiliensis and contribute to a delayed protective immune response, modulating late-stage inflammatory containment and bacterial clearance in experimental mycetoma.
METHODS: Using MCdeficient KitW-sh/W-sh mice, this study investigated the role of mast cells (MCs) in a murine model of actinomycetoma. Clinical progression, bacterial burden, histopathology, and lesional leukocyte infiltration were analyzed at 30 and 72 days postinfection, and bone marrowderived MCs were challenged in vitro with Nocardia brasiliensis to assess activation.
RESULTS: MC-deficient mice exhibited a significant increase in bacterial load concomitant with attenuated late-phase (72-day) inflammation, characterized by reduced lesional neutrophilia and lymphocytic infiltration. Furthermore, MC absence disrupted the characteristic morphology of bacterial grains. In vitro, N. brasiliensis induced potent MC degranulation and pro-inflammatory cytokine release.
CONCLUSIONS: These data demonstrate that MCs are directly activated by N. brasiliensis and contribute to a delayed protective immune response, modulating late-stage inflammatory containment and bacterial clearance in experimental mycetoma.