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Background  Eosinophilic meningitis, caused by fifth-stage larvae of the nematode (roundworm)  Angiostrongylus cantonensis , is mainly attributed to the contribution of eosinophils to tissue inflammatory responses in helminthic infections. Eosinophils are associated with the killing of helminths via peroxidative oxidation and hydrogen peroxide generated by the dismutation of superoxide produced during respiratory bursts. In contrast, when residing in the host with high level of eosinophils, helminthic worms have evolved to attenuate eosinophil-mediated tissue inflammatory responses for their survival in the hosts. In a previous study we demonstrated that the expression of the  A. cantonensis  RPS 30 gene ( Acan - rps- 30) was significantly downregulated in  A. cantonensis  L5 roundworms residing in cerebrospinal fluid with a high level of eosinophils.  Acan -RPS-30 is a protein homologous to the human Fau protein that plays a pro-apoptotic regulatory role and may function in protecting worms from oxidative stress.    Methods  The isolation and structural characterization of  Acan -RPS-30 were performed using rapid amplification of cDNA ends (RACE), genome walking and bioinformatics. Quantitative real-time-PCR and microinjection were used to detect the expression patterns of  Acan-rps- 30. Feeding RNA interference (RNAi) was used to knockdown the apoptosis gene  ced-3 . Microinjection was performed to construct transgenic worms. An oxidative stress assay was used to determine the functions of  Acan -RPS-30.    Results  Our results showed that  Acan- RPS-30 consisted of 130 amino acids. It was grouped into clade V with  C. elegans  in the phylogenetic analysis. It was expressed ubiquitously in worms and was downregulated in both L5 larvae and adult  A. cantonensis . Worms expressing  pCe-rps 30 ::Acan-rps- 30 ::rfp , with the refractile “button-like” apoptotic corpses, were susceptible to oxidative stress. Apoptosis genes  ced- 3 and  ced- 4 were both upregulated in the transgenic worms. The phenotype susceptible to oxidative stress could be converted with a  ced- 3 defective mutation and RNAi.  rps- 30 −/−  mutant worms were resistant to oxidative stress, with  ced- 3 and  ced- 4 both downregulated. The oxidative stress-resistant phenotype could be rescued and inhibited by through the expression of  pCe-rps 30 ::Acan-rps- 30 ::rfp  in  rps- 3 −/−  mutant worms.    Conclusion  In  C. elegans  worms, downregulated RPS-30 plays a defensive role against damage due to oxidative stress, facilitating worm survival by regulating downregulated  ced-3 . This observation may indicate the mechanism by which  A. cantonensis  L5 worms, with downregulated  Acan- RPS-30, survive in the central nervous system of humans from the immune response of eosinophils.    Graphic abstract

Downregulated RPS-30 in Angiostrongylus cantonensis L5 plays a defensive role against damage due to oxidative stress