Comparative neuropathogenesis of Angiostrongylus cantonensis and Angiostrongylus malaysiensis infection in an experimental BALB/c mouse model
Issued Date
2026-07-01
Resource Type
ISSN
0001706X
eISSN
18736254
Scopus ID
2-s2.0-105038044218
Pubmed ID
42069170
Journal Title
Acta Tropica
Volume
279
Rights Holder(s)
SCOPUS
Bibliographic Citation
Acta Tropica Vol.279 (2026)
Suggested Citation
Charoennitiwat V., Sukwattananipaat P., Ratnarathorn N., Pewla-oo S., Viriyautsahakul S., Thongsom C., Poonpok S., Saechong Y., Ongnok B., Thaenkham U., Limjunyawong N. Comparative neuropathogenesis of Angiostrongylus cantonensis and Angiostrongylus malaysiensis infection in an experimental BALB/c mouse model. Acta Tropica Vol.279 (2026). doi:10.1016/j.actatropica.2026.108113 Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/116742
Title
Comparative neuropathogenesis of Angiostrongylus cantonensis and Angiostrongylus malaysiensis infection in an experimental BALB/c mouse model
Corresponding Author(s)
Other Contributor(s)
Abstract
Neuroangiostrongyliasis is a neuroinvasive helminth infection caused primarily by the rat lungworm Angiostrongylus cantonensis, which is the main causative agent of eosinophilic meningitis in humans. The closely related species Angiostrongylus malaysiensis coexists in many endemic regions particularly in Asia and Oceania and shares substantial morphological and genetic similarity with A. cantonensis, yet its pathogenic potential remains poorly understood. Here, we performed a direct comparative investigation of neuropathogenesis and host immune responses following experimental infection with A. cantonensis or A. malaysiensis in a murine model. Both species established central nervous system infection and induced neurological manifestations and inflammatory responses. However, infection with A. malaysiensis resulted in more severe clinical disease, characterized by greater weight loss, higher clinical scores, and extensive cerebral hemorrhage, accompanied by increased parasite invasion into the brain parenchyma. In contrast, A. cantonensis infection elicited stronger neuroimmune activation, including increased leukocyte recruitment and elevated expression of type 2 cytokines and chemokines within the brain and meninges. Despite the more severe neurological complications observed in A. malaysiensis infection, immune cell accumulation in the central nervous system was comparatively reduced, suggesting differences in parasite containment at the neuroimmune interface. Together, these findings demonstrate that closely related Angiostrongylus species can induce distinct patterns of neuropathogenesis and immune regulation. Our results highlight the importance of species-specific host–parasite interactions in shaping disease severity and provide new insight into mechanisms underlying the pathogenesis of neuroangiostrongyliasis.