The effect of immunosuppression on secondary Echinococcus multilocularis infections in mice

Baron, Régis; Tanner, C. E.

doi:10.1016/0020-7519(76)90008-4

Cited by 65 publications

(21 citation statements)

References 28 publications

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“…Impairment of cellular immunity (immune suppression) is followed by an increase in susceptibility to E. multilocularis in experimental animals. This was shown more than 30 years ago in immunosuppressed mice by Baron and Tanner [12] and was further demonstrated later on using SCID mice, which were shown to be highly susceptible compared to the wild strain and to reconstituted mice [13], and in nude mice [14]. A similar increase of susceptibility of experimental mice, associated with a decrease of delayed type hypersensitivity, was also observed in mice infected with E. multilocularis and treated with an immunosuppressive drug, cyclosporine, which interferes with IL-2 production in T-cells [15].…”

Section: Susceptibility and Resistance Of Animal Intermediate Hostmentioning

confidence: 72%

Echinococcus multilocularisand Its Intermediate Host: A Model of Parasite-Host Interplay

Vuitton

Gottstein

2010

Journal of Biomedicine and Biotechnology

141

172

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Host-parasite interactions in the E. multilocularis-intermediate host model depend on a subtle balance between cellular immunity, which is responsible for host's resistance towards the metacestode, the larval stage of the parasite, and tolerance induction and maintenance. The pathological features of alveolar echinococcosis. the disease caused by E. multilocularis, are related both to parasitic growth and to host's immune response, leading to fibrosis and necrosis, The disease spectrum is clearly dependent on the genetic background of the host as well as on acquired disturbances of Th1-related immunity. The laminated layer of the metacestode, and especially its carbohydrate components, plays a major role in tolerance induction. Th2-type and anti-inflammatory cytokines, IL-10 and TGF-β, as well as nitric oxide, are involved in the maintenance of tolerance and partial inhibition of cytotoxic mechanisms. Results of studies in the experimental mouse model and in patients suggest that immune modulation with cytokines, such as interferon-α, or with specific antigens could be used in the future to treat patients with alveolar echinococcosis and/or to prevent this very severe parasitic disease.

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Section: Susceptibility and Resistance Of Animal Intermediate Hostmentioning

confidence: 72%

Echinococcus multilocularisand Its Intermediate Host: A Model of Parasite-Host Interplay

Vuitton

Gottstein

2010

Journal of Biomedicine and Biotechnology

141

172

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“…An interesting feature observed in chronic AE is a marked depression of the cell-mediated immune response [61], [62], [63]. These general characteristics of E. multilocularis , including the seemingly tumor like growth, its ability to modulate host immune responses, and the fact that in vitro culture is an established technique, renders this parasite a very attractive model to study the host-parasite interplay in view to reveal potentially novel modes of therapy [56].…”

Section: Discussionmentioning

confidence: 99%

Hepatic Gene Expression Profile in Mice Perorally Infected with Echinococcus multilocularis Eggs

et al. 2010

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BackgroundAlveolar echinococcosis (AE) is a severe chronic hepatic parasitic disease currently emerging in central and eastern Europe. Untreated AE presents a high mortality (>90%) due to a severe hepatic destruction as a result of parasitic metacestode proliferation which behaves like a malignant tumor. Despite this severe course and outcome of disease, the genetic program that regulates the host response leading to organ damage as a consequence of hepatic alveolar echinococcosis is largely unknown.Methodology/Principal FindingsWe used a mouse model of AE to assess gene expression profiles in the liver after establishment of a chronic disease status as a result of a primary peroral infection with eggs of the fox tapeworm Echinococcus multilocularis. Among 38 genes differentially regulated (false discovery rate adjusted p≤0.05), 35 genes were assigned to the functional gene ontology group , while 3 associated with the functional group . Upregulated genes associated with could be clustered into functional subgroups including , , , and . Two downregulated genes related to and , respectively. The genes either associated with an or an pathway. From the overexpressed genes, 18 genes were subsequently processed with a Custom Array microfluidic card system in order to assess respective expression status at the mRNA level relative to 5 reference genes (Gapdh, Est1, Rlp3, Mdh-1, Rpl37) selected upon a constitutive and stable expression level. The results generated by the two independent tools used for the assessment of gene expression, i.e., microarray and microfluidic card system, exhibited a high level of congruency (Spearman correlation rho = 0.81, p = 7.87e-5) and thus validated the applied methods.Conclusions/SignificanceBased on this set of biomarkers, new diagnostic targets have been made available to predict disease status and progression. These biomarkers may also offer new targets for immuno-therapeutic intervention.

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“…Immunocompetent mice respond immunologically, but in a strain-dependent manner (Matsumoto et al, 2010). It was shown that impairment of cellular immunity (immune suppression) in mice is followed by an increase in susceptibility to E. multilocularis (Baron and Tanner, 1976) and this was further confirmed in SCID mice (Playford and Kamiya, 1992) and in nude mice (Dai et al, 2004). A similar increase of susceptibility, associated with a decrease of delayed type hypersensitivity was also observed in E. multilocularis infected mice treated with ciclosporin, which interferes in IL-2 production by Tcells (Liance et al, 1992).…”

Section: Biology and Immunology Of Susceptibility Versus Resistance Imentioning

confidence: 98%

Susceptibility versus resistance in alveolar echinococcosis (larval infection with Echinococcus multilocularis)

Gottstein

Wang

Boubaker

et al. 2015

Veterinary Parasitology

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Epidemiological studies have demonstrated that the majority of human individuals exposed to infection with Echinococcus spp. eggs exhibit resistance to disease as shown by either seroconversion to parasite--specific antigens, and/or the presence of 'dying out' or 'aborted' metacestodes, not including hereby those individuals who putatively got infected but did not seroconvert and who subsequently allowed no development of the pathogen. For those individuals where infection leads to disease, the developing parasite is partially controlled by host immunity. In infected humans, the type of immune response developed by the host accounts for the subsequent trichotomy concerning the parasite development: (i) seroconversion proving infection, but lack of any hepatic lesion indicating the failure of the parasite to establish and further develop within the liver; or resistance as shown by the presence of fully calcified lesions; (ii) controlled susceptibility as found in the "conventional" alveolar echinococcosis (AE) patients who experience clinical signs and symptoms approximately 5-15 years after infection, and (iii) uncontrolled hyperproliferation of the metacestode due to an impaired immune response (AIDS or other immunodeficiencies). Immunomodulation of host immunity toward anergy seems to be triggered by parasite metabolites. Beside immunomodulating IL-10, TGFβ-driven regulatory T cells have been shown to play a crucial role in the parasite-modulated progressive course of AE. A novel CD4+CD25+ Treg effector molecule FGL2 recently yielded new insight into the tolerance process in Echinococcus multilocularis infection.

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The effect of immunosuppression on secondary Echinococcus multilocularis infections in mice

Cited by 65 publications

References 28 publications

Echinococcus multilocularisand Its Intermediate Host: A Model of Parasite-Host Interplay

Echinococcus multilocularisand Its Intermediate Host: A Model of Parasite-Host Interplay

Hepatic Gene Expression Profile in Mice Perorally Infected with Echinococcus multilocularis Eggs

Susceptibility versus resistance in alveolar echinococcosis (larval infection with Echinococcus multilocularis)

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