Angiostrongylus cantonensis daf-2 regulates dauer, longevity and stress in Caenorhabditis elegans

Yan, Bowen; Sun, Weiwei; Shi, Xiaomeng; Huang, Liyang; Chen, Lingzi; Wang, Suhua; Yan, Lanzhu; Liang, Shuli; Huang, Huicong

doi:10.1016/j.vetpar.2017.04.025

Cited by 6 publications

(10 citation statements)

References 45 publications

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“…A. cantonensis is relatively closely related to the model organism C. elegans, both belonging to clade V [2,34], and the homologous gene of Acan-rps-30 is Ce-rps30 (C26F1.4). Here, we used C. elegans as a surrogate to explore the in vivo functions of the homologous gene, Acan-rps-30, for the lack of effective genetic manipulation in parasitic nematode.…”

Section: Discussionmentioning

confidence: 99%

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

Sun

Yan

Shi

et al. 2020

Preprint

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Background: Eosinophilic meningitis, caused by Angiostrongylus cantonensis L5, is mainly attributed to the Eosinophils, which contribute to tissue inflammatory responses in helminthic infections. Eosinophils are associated with helminthic killing, using the peroxidative oxidation and hydrogen peroxide (H2O2) generated by dismutation of superoxide produced during respiratory burst. In contrast, residing in the host with high level of eosinophils, helminthic worms have evolved to attenuate eosinophil-mediated tissue inflammatory responses for their survival in hosts. Our previous study demonstrated that the expression of Acan-rps-30 was significantly down-regulated in A. cantonensis L5 worms, which reside in the cerebrospinal fluid with high level of Eosinophils. Acan-RPS-30, a homologous protein of human Fau, which plays a pro-apoptotic regulatory role, may function in protecting worms from oxidative stress.Methods: RACE, genome Walking, bioinformatics were used to isolate and analyse the structural characterisation of Acan-RPS-30; qRT-PCR and microinjection was performed to detect the expression patterns of Acan-rps-30; feeding RNAi was used to ced-3 knock-down; microinjection was performed to construct transgenic worms; 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, and was grouped into Clade V with C. elegans in phylogenetic analysis. It was expressed ubiquitously in worms and was down-regulated in both L5 and adult A. cantonensis. Worms expressing pCe-rps30::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 up-regulated in the transgenic worms. And the phenotype susceptible to oxidative stress could be converted with ced-3 defective mutation and RNAi. rps-30- /- mutant worms were resistant to oxidative stress, with ced-3 and ced-4 were both down-regulated. And the oxidative stress resistance phenotype could be rescued and inhibited by expressing pCe-rps30::Acan-rps-30::rfp in rps-30- /- mutant worms. Conclusion: In C. elegans worms, down-regulated RPS-30 plays a defensive role against damage due to oxidative stress for worm survival by regulating ced-3 down-regulated. And this might indicate the mechanism of A. cantonensis L5 worms, with Acan-RPS-30 down-regulated, surviving in the central nervous system of human from immune attack of Eosinophil.

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Section: Discussionmentioning

confidence: 99%

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

Sun

Yan

Shi

et al. 2020

Preprint

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“…Recombinant plasmids were each microinjected into the gonad of young, adult C. elegans hermaphrodites as described previously [2,30], together with plasmid pRF4 containing a dominant mutant allele of the rol-6 gene, each at a final concentration of 50 μg/ml in the same mixture, using the pPD95.77 (pCe-rps30::gfp) and pRF4 plasmid mixture as a control. The F2 and subsequent generations with a roller phenotype were analyzed and selected to examine the expression patterns of green fluorescent protein (GFP) or red fluorescent protein (RFP), using a fluorescent microscope (Olympus model IX71; Olympus Corp., Tokyo, Japan).…”

Section: Transgenic Wormsmentioning

confidence: 99%

“…Several different hosts are required to complete the life-cycle of A. cantonensis. Humans are an atypical host are are mainly be infected through accidental ingestion of undercooked intermediate hosts, such as the golden apple/ channeled apple snail Pomacea canaliculata in which the infective third-stage larvae (iL3) resides [2]. After passage to the small intestine, iL3 will penetrate the blood-brain barrier, subsequently infecting the central nervous system where it will develop into the fifth-stage larvae (L5) and cause angiostrongyliasis with neurological symptoms [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

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

et al. 2020

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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-rps30::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-rps30::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

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“…Recombinant plasmids were each microinjected into the gonad of young, adult C. elegans hermaphrodites as described [2,30], together with plasmid pRF4 containing a dominant mutant allele of rol-6 gene, each at a nal concentration of 50 µg/mL in the same mixture, using pPD95.77 (pCe-rps30::gfp) and pRF4 plasmid mixture as a control. The F2 and subsequent generations with a roller phenotype were analyzed and selected to examine the expression patterns of GFP or RFP, using a uorescent microscope (Olympus IX71).…”

Section: Transgenic Wormsmentioning

confidence: 99%

“…Several different hosts are required to complete the life cycle of A. cantonensis. Human, as an abnormal host, can mainly be infected by accidental ingestion of undercooked intermediate hosts, such as Pomacea canaliculata, in which the infective third-stage larvae (iL3) resides [2]. After passage to the small intestine, iL3 will penetrate the blood-brain barrier, and then affects the central nervous system, where it will develop into the fth-stage larvae (L5), causing Angiostrongyliasis with neurological symptoms [3][4][5][6].…”

Section: Introductionmentioning

confidence: 99%

Down-regulated RPS-30 in Angiostrongylus Cantonensis L5 Plays a Defensive Role Against Damage Due to Oxidative Stress

Sun

Yan

Shi

et al. 2020

Preprint

Self Cite

View full text Add to dashboard Cite

Background: Eosinophilic meningitis, caused by Angiostrongylus cantonensis L5, is mainly attributed to the Eosinophils, which contribute to tissue inflammatory responses in helminthic infections. Eosinophils are associated with helminthic killing, using the peroxidative oxidation and hydrogen peroxide (H2O2) generated by dismutation of superoxide produced during respiratory burst. In contrast, residing in the host with high level of eosinophils, helminthic worms have evolved to attenuate eosinophil-mediated tissue inflammatory responses for their survival in hosts. Our previous study demonstrated that the expression of Acan-rps-30 was significantly down-regulated in A. cantonensis L5 worms, which reside in the cerebrospinal fluid with high level of Eosinophils. Acan-RPS-30, a homologous protein of human Fau, which plays a pro-apoptotic regulatory role, may function in protecting worms from oxidative stress.Methods: RACE, genome Walking, bioinformatics were used to isolate and analyse the structural characterisation of Acan-RPS-30; qRT-PCR and microinjection was performed to detect the expression patterns of Acan-rps-30; feeding RNAi was used to ced-3 knock-down; microinjection was performed to construct transgenic worms; 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, and was grouped into Clade V with C. elegans in phylogenetic analysis. It was expressed ubiquitously in worms and was down-regulated in both L5 and adult A. cantonensis. Worms expressing pCe-rps30::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 up-regulated in the transgenic worms. And the phenotype susceptible to oxidative stress could be converted with ced-3 defective mutation and RNAi. rps-30- /- mutant worms were resistant to oxidative stress, with ced-3 and ced-4 were both down-regulated. And the oxidative stress resistance phenotype could be rescued and inhibited by expressing pCe-rps30::Acan-rps-30::rfp in rps-30- /- mutant worms. Conclusion: In A. cantonensis L5 worms, down-regulated Acan-RPS-30 plays a defensive role against damage due to oxidative stress for worm survival through inhibiting apoptosis by regulating ced-3 down-regulated.

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Angiostrongylus cantonensis daf-2 regulates dauer, longevity and stress in Caenorhabditis elegans

Cited by 6 publications

References 45 publications

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

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

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

Down-regulated RPS-30 in Angiostrongylus Cantonensis L5 Plays a Defensive Role Against Damage Due to Oxidative Stress

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