Physiological stress responses and dynamics of corticosterone levels during Angiostrongylus cantonensis infection in mice

Parasitic infections commonly trigger host stress responses, primarily through activation of hypothalamic‒pituitary‒adrenal (HPA) axis, leading to increased glucocorticoid secretion, with variations depending on the infectious agent. However, the physiological stress induced by Angiostrongylus cantonensis , the causative agent of eosinophilic meningitis (EOM), remains insufficiently characterized. In this study, we comprehensively investigated glucocorticoid dynamics and stress-related responses in BALB/c mice experimentally infected with A . cantonensis over four weeks. Corticosterone levels in both serum and hair were measured using ELISA. Additionally, locomotor activity and anxiety-like behavior were assessed using the open field test (OFT), and adrenal glucocorticoid synthesis gene expression was analyzed by RT-qPCR. Our results revealed a significant progressive increase in hair corticosterone (HC) over time in infected mice compared with controls, whereas serum corticosterone levels fluctuated. Although locomotor activity showed an inconsistent trend, infected mice tended toward increased anxiety-like behavior. The expression of steroidogenic genes ( Crh , Mc2r , Cyp11b1 , Hsd11b1 , and Hsd11b2 ) was notably upregulated during the mid-infection period, but then declined. These findings indicate that A. cantonensis infection in mice induces a measurable physiological stress response, marked by glucocorticoid elevation and changes adrenal steroidogenesis-related gene expression—even in the absence of observable behavioral changes. Notably, the progressive rise in HC supports its use as a reliable, noninvasive biomarker for chronic stress. However, its relevance to zoonotic disease monitoring is limited, as HC is a nonspecific indicator influenced by many unrelated factors and cannot be directly linked to specific infections.