Abstract
<title>Abstract</title> <p> <italic>Angiostrongylus cantonensis</italic> infection causes severe eosinophilic meningoencephalitis, characterized by intense neuroinflammation and mechanical tissue damage. Sirtuin-1 has been reported to exert neuroprotective effects in this disease context. In this study, sirtuin-1 silencing is sufficient to induce NF-κB activation and subsequent apoptosis in microglial cells stimulated with excretory–secretory products (ESPs) of <italic>A. cantonensis</italic> . Furthermore, we investigated the role of miR-155-5p in ESPs-stimulated microglial cells and <italic>A. cantonensis</italic> -infected mice. The results showed that miR-155-5p expression was significantly upregulated in both models. Notably, dual-luciferase reporter assays confirmed that miR-155-5p directly targets the 3´untranslated region (3´UTR) of sirtuin-1, leading to its downregulation. Overexpression of miR-155-5p markedly increased levels of phosphorylated p65 (p-p65) and pro-apoptotic markers, including caspase-3 and Bax, while reducing the expression of anti-apoptotic proteins such as Bcl-2 and IAP-1. These findings indicate that the miR-155-5p/sirtuin-1/NF-κB signaling axis plays a critical role in mediating apoptosis during <italic>A. cantonensis</italic> infection. Overall, this study identifies miR-155-5p as a potential biomarker and key regulator of apoptosis in eosinophilic meningoencephalitis, acting through its interaction with sirtuin-1. </p>