The mRNA level of the galectin-10 of Angiostrongylus cantonensis induced by reactive oxygen stress

Liu, Ling-hui; He, Hailong; Lv, Zhi-yue; Wei, Jie; Zeng, Xiaofeng; Liang, Jinyi; Zheng, Haixue; Yu, Xinbing; Sun, Xi; Wu, Zhongdao

doi:10.1007/s00436-012-3210-5

Cited by 12 publications

(7 citation statements)

References 20 publications

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“…Previous studies have shown that the invasion of the central nervous system (CNS) by developing larvae of the parasite can cause eosinophilic inflammation [ 7 – 9 ]. The larvae generally remain in the CNS and eosinophil recruitment can cause neuropathological damage [ 10 – 13 ].…”

Section: Introductionmentioning

confidence: 99%

Preliminary expression profile of cytokines in brain tissue of BALB/c mice with Angiostrongylus cantonensis infection

Wei

et al. 2015

Parasites Vectors

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BackgroundAngiostrongylus cantonensis (A. cantonensis) infection can result in increased risk of eosinophilic meningitis. Accumulation of eosinophils and inflammation can result in the A. cantonensis infection playing an important role in brain tissue injury during this pathological process. However, underlying mechanisms regarding the transcriptomic responses during brain tissue injury caused by A. cantonensis infection are yet to be elucidated. This study is aimed at identifying some genomic and transcriptomic factors influencing the accumulation of eosinophils and inflammation in the mouse brain infected with A. cantonensis.MethodsAn infected mouse model was prepared based on our laboratory experimental process, and then the mouse brain RNA Libraries were constructed for deep Sequencing with Illumina Genome Analyzer. The raw data was processed with a bioinformatics’ pipeline including Refseq genes expression analysis using cufflinks, annotation and classification of RNAs, lncRNA prediction as well as analysis of co-expression network. The analysis of Refseq data provides the measure of the presence and prevalence of transcripts from known and previously unknown genes.ResultsThis study showed that Cys-Cys (CC) type chemokines such as CCL2, CCL8, CCL1, CCL24, CCL11, CCL7, CCL12 and CCL5 were elevated significantly at the late phase of infection. The up-regulation of CCL2 indicated that the worm of A. cantonensis had migrated into the mouse brain at an early infection phase. CCL2 could be induced in the brain injury during migration and CCL2 might play a major role in the neuropathic pain caused by A. cantonensis infection. The up-regulated expression of IL-4, IL-5, IL-10, and IL-13 showed Th2 cell predominance in immunopathological reactions at late infection phase in response to infection by A. cantonensis. These different cytokines can modulate and inhibit each other and function as a network with the specific potential to drive brain eosinophilic inflammation. The increase of ATF-3 expression at 21 dpi suggested the injury of neuronal cells at late phase of infection. 1217 new potential lncRNA were candidates of interest for further research.ConclusionsThese cytokine networks play an important role in the development of central nervous system inflammation caused by A. cantonensis infection.Electronic supplementary materialThe online version of this article (doi:10.1186/s13071-015-0939-6) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

Preliminary expression profile of cytokines in brain tissue of BALB/c mice with Angiostrongylus cantonensis infection

Wei

et al. 2015

Parasites Vectors

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“…We reported that soluble antigens derived from stage- IV A.C . larvae contain various proteins that play diverse functions during infection [ 19 , 26 , 45 ]. In our study, sAgs from A.C .…”

Section: Discussionmentioning

confidence: 99%

Soluble antigens from the neurotropic pathogenAngiostrongylus cantonensisdirectly induce thymus atrophy in a mouse model

Liu

et al. 2017

Oncotarget

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The nematode Angiostrongylus cantonensis (A.C.) is a neurotropic pathogen; stage-III larva invade the human (non-permissive host) central nervous system (CNS) to cause eosinophilic meningitis or meningoencephalitis accompanied by immunosuppression. In an A.C.-infectedmouse (another non-permissive host) model, CNS damage-associated T cell immune deficiency and severe inflammation were proposed to result from activation of the hypothalamic-pituitary-adrenal (HPA) axis. However, glucocorticoids are anti-inflammatory agents. Additionally, while defects in thymic stromal/epithelial cells (TECs) are the major reason for thymic atrophy, TECs do not express the glucocorticoid receptor. Therefore, activation of the HPA axis cannot fully explain the thymic atrophy and inflammation. Using an A.C.-infected mouse model, we found that A.C.-infected mice developed severe thymic atrophy with dramatic impairments in thymocytes and TECs, particularly cortical TECs, which harbor CD4+CD8+ double-positive thymocytes. The impairments resulted from soluble antigens (sAgs) from A.C. in the thymuses of infected mice, as intrathymic injection of these sAgs into live mice and the addition of these sAgs to thymic cell culture resulted in thymic atrophy and cellular apoptosis, respectively. Therefore, in addition to an indirect effect on thymocytes through the HPA axis, our study reveals a novel mechanism by which A.C. infection in non-permissive hosts directly induces defects in both thymocytes and TECs via soluble antigens.

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“…As no function has yet been attributed to parasite galectins, it has been speculated that they may be involved in host–parasite interaction . For example, a galectin from Angiostronglylus cantonensis plays a role in the activation of microglia, but the mechanism is unknown . Moreover, current evidence suggests that parasite galectins participate actively in the infection process as pattern‐recognition receptors (PRRs) .…”

Section: Discussionmentioning

confidence: 99%

Galectin isolated from parasite inhibits remission of experimental autoimmune encephalomyelitis by up-regulating autoantibody

Bing

Ahn

et al. 2015

Clinical and Experimental Immunology

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SummaryRecently, parasite infections or parasite-derived products have been suggested as a therapeutic strategy with suppression of immunopathology, which involves the induction of regulatory T cells or/and T helper type 2 (Th2) responses. In a recent study, researchers reported that constructed recombinant galectin (rTl-gal) isolated from an adult worm of the gastrointestinal nematode parasite Toxascaris leonina attenuated clinical symptoms of inflammatory bowel disease in mice treated with dextran sulphate sodium. Noting the role of rTl-gal in inflammatory disease, we attempted to investigate the effect of the parasite via its rTl-gal on neuronal autoimmune disease using experimental autoimmune encephalomyelitis (EAE), a mouse inflammatory and demyelinating autoimmune disease model of human multiple sclerosis. In this model, rTl-gal-treated experimental autoimmune encephalomyelitis (EAE) mice failed to recover after the peak of the disease, leading to persistent central nervous system (CNS) damage, such as demyelination, gliosis and axonal damage. Further, rTl-gal-treated EAE mice markedly increased the number of CD45R/B220 1 B cells in both infiltrated inflammation and the periphery, along with the increased production of autoantibody [antimyelin oligodendrocyte glycoprotein (MOG) ] in serum at chronic stage. Upon antigen restimulation, rTl-gal treatment affected the release of overall cytokines, especially interferon (IFN)-g and tumour necrosis factor (TNF)-a. Our results suggest that galectin isolated from a gastrointestinal parasite can deliver a harmful effect to EAE contrary to its beneficial effect on inflammatory bowel disease.

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The mRNA level of the galectin-10 of Angiostrongylus cantonensis induced by reactive oxygen stress

Cited by 12 publications

References 20 publications

Preliminary expression profile of cytokines in brain tissue of BALB/c mice with Angiostrongylus cantonensis infection

Preliminary expression profile of cytokines in brain tissue of BALB/c mice with Angiostrongylus cantonensis infection

Soluble antigens from the neurotropic pathogenAngiostrongylus cantonensisdirectly induce thymus atrophy in a mouse model

Galectin isolated from parasite inhibits remission of experimental autoimmune encephalomyelitis by up-regulating autoantibody

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