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However, the explicit underlying molecular basis of apoptosis and necroptosis upon AC infection has not yet been elucidated. To determine the specific pathways of apoptosis and necroptosis upon AC infection, gene set enrichment analysis (GSEA) and protein\u2013protein interaction (PPI) analysis for gene expression microarray (accession number: GSE159486) of mouse brain infected by AC revealed that TNF-\u03b1 likely played a central role in the apoptosis and necroptosis in the context of AC infection, which was further confirmed via an in vivo rescue assay after treating with TNF-\u03b1 inhibitor. The signalling axes involved in apoptosis and necroptosis were investigated via immunoprecipitation and immunoblotting. Immunofluorescence was used to identify the specific cells that underwent apoptosis or necroptosis. The results showed that TNF-\u03b1 induced apoptosis of astrocytes through the RIP1\/FADD\/Caspase-8 axis and induced necroptosis of neurons by the RIP3\/MLKL signalling pathway. In addition, in vitro assay revealed that TNF-\u03b1 secretion by microglia increased upon LSA stimulation and caused necroptosis of neurons. The present study provided the first evidence that TNF-\u03b1 was secreted by microglia stimulated by AC infection, which caused cell death via parallel pathways of astrocyte apoptosis (mediated by the RIP1\/FADD\/caspase-8 axis) and neuron necroptosis (driven by the RIP3\/MLKL complex). Our research comprehensively elucidated the mechanism of cell death after AC infection and provided new insight into targeting TNF-\u03b1 signalling as a therapeutic strategy for CNS injury.<\/jats:p>","DOI":"10.1007\/s10571-021-01063-w","type":"journal-article","created":{"date-parts":[[2021,3,8]],"date-time":"2021-03-08T11:02:49Z","timestamp":1615201369000},"page":"1841-1857","update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":43,"title":["TNF-\u03b1 Triggers RIP1\/FADD\/Caspase-8-Mediated Apoptosis of Astrocytes and RIP3\/MLKL-Mediated Necroptosis of Neurons Induced by Angiostrongylus cantonensis Infection"],"prefix":"10.1007","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3004-8481","authenticated-orcid":false,"given":"Hongli","family":"Zhou","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2596-2778","authenticated-orcid":false,"given":"Minyu","family":"Zhou","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-2783-7751","authenticated-orcid":false,"given":"Yue","family":"Hu","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-4027-3412","authenticated-orcid":false,"given":"Yanin","family":"Limpanon","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8912-3132","authenticated-orcid":false,"given":"Yubin","family":"Ma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5699-0934","authenticated-orcid":false,"given":"Ping","family":"Huang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2192-3969","authenticated-orcid":false,"given":"Paron","family":"Dekumyoy","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-6726-3759","authenticated-orcid":false,"given":"Wanchai","family":"Maleewong","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-1792-2805","authenticated-orcid":false,"given":"Zhiyue","family":"Lv","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2021,3,8]]},"reference":[{"key":"1063_CR1","doi-asserted-by":"publisher","first-page":"3263","DOI":"10.1038\/onc.2012.337","volume":"32","author":"BA Abhari","year":"2013","unstructured":"Abhari BA, Cristofanon S, Kappler R, von Schweinitz D, Humphreys R, Fulda S (2013) RIP1 is required for IAP inhibitor-mediated sensitization for TRAIL-induced apoptosis via a RIP1\/FADD\/caspase-8 cell death complex. 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