Introduction The ability of Echinococcus multilocularis (E.m) to establish infection depends on evading host immune clearance during the early stages. This study investigated the mechanisms by which host macrophages eliminate E.m during this critical window. Methods We utilized a mouse infection model with fluorescently labeled protoscoleces to observe early immune dynamics in vivo . Histopathological analysis was performed to characterize lesion phenotypes. The mechanism of parasite killing was further explored using in vitro co-culture experiments and scanning electron microscopy (SEM). Results Rapid immune cell infiltration and parasite clearance in the liver were observed within 24 hours post-infection. Histopathological analysis revealed two distinct lesion phenotypes: "Progressive Lesions," characterized by a failure of macrophage infiltration and parasite transformation into vesicles, and "Regressive Lesions," marked by high macrophage density and complete parasite elimination. In vitro experiments demonstrated that macrophages mediated protoscolex killing through complement-dependent trogocytosis, a process requiring active serum components. SEM confirmed direct macrophage-parasite contact and trogocytosis as the primary mode of elimination. Discussion These findings highlight the pivotal role of macrophage trogocytosis in early host defense against E.m infection and provide new insights into the mechanisms of innate immunity in parasitic clearance.
Yang et al. (Thu,) studied this question.