Experimental Disseminated Strongyloidiasis in Erythrocebus patas

Genta, Robert M.; London, William I.; Gam, Albert A.; Harper, James S.; Neva, Franklin A.

doi:10.4269/ajtmh.1984.33.444

Cited by 26 publications

(14 citation statements)

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“…A few studies have addressed the role of S. stercoralisspecific antibody responses in regulating larval output, and these have reported no association between parasitological and immunological parameters (Genta et al 1984, 1986, Sato et al 1985. These studies typically describe the levels of antibody responses to crude larval extracts measured by ELISA.…”

Section: Discussionmentioning

confidence: 99%

“…Whilst host immunocompetence is likely to be the primary regulator of infection levels in autoinfective strongyloidiasis, there is little experimental evidence to support this hypothesis (Genta 1992). Several studies, which would offer further insight into the regulation of infection, have failed to demonstrate a link between host immune status and parasitological or clinical parameters (Genta et al 1984, 1986, Sato et al 1985, Badaró et al 1987). An alternative hypothesis is that regulation of the rate of autoinfection may primarily be affected by endocrine control of the rate of larval moulting (Genta 1992).…”

Section: Introductionmentioning

confidence: 99%

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L3 antigen‐specific antibody isotype responses in human strongyloidiasis: correlations with larval output

Atkins

Conway

Lindo

et al. 1999

Parasite Immunology

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Autoinfective strongyloidiasis is potentially fatal, yet the majority of infected individuals harbour asymptomatic and chronic infections. The role of humoral responses in modulating autoinfection was assessed by examining antibody isotype responses to filariform larval antigens amongst chronically infected ex-Far East Prisoners of War (exFEPOWs) with longstanding (> 30 years) infection. Serum immunoglobulin (Ig)G1, IgG4, IgE and IgA responses to whole Strongyloides stercoralis L3 extracts and their constituent antigenic components were characterized by ELISA and quantitative immunoblotting. Comparison of two groups of S. stercoralis infected exFEPOWs with and without detectable larvae in stool demonstrated novel trends. Significantly enhanced recognition of six immunodominant antigenic components by IgA was associated with undetectable larval output, as was enhanced IgE recognition of several components. Additionally, IgE and IgG4 exhibited parallel antigen recognition patterns. These findings are consistent with roles for IgA in modulating larval output, for IgE in regulating autoinfection, and for IgG4 in blocking IgE-mediated responses in human strongyloidiasis.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

L3 antigen‐specific antibody isotype responses in human strongyloidiasis: correlations with larval output

Atkins

Conway

Lindo

et al. 1999

Parasite Immunology

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“…These findings suggest that antibody and eosinophils play a role in protective immunity to larval S. stercoralis in humans (5). In Erythrocebus patas monkeys and dogs infected with S. stercoralis, elevated anti-larval IgG titers were observed; however, it was not determined whether the elevated antibody titers were related to decreases in parasite survival (9,12). Jirds can also support the complete S. stercoralis life cycle.…”

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confidence: 98%

Specificity and Mechanism of Immunoglobulin M (IgM)-and IgG-Dependent Protective Immunity to LarvalStrongyloides stercoralisinMice

et al. 2003

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Protective immunity in mice to the infective third-stage larvae (L3) of Strongyloides stercoralis was shown to be dependent on immunoglobulin M (IgM), complement activation, and granulocytes. The objectives of the present study were to determine whether IgG was also a protective antibody isotype and to define the specificity and the mechanism by which IgG functions. Purified IgG recovered from mice 3 weeks after a booster immunization with live L3 was shown to transfer high levels of protective immunity to naïve mice. IgG transferred into mice treated to block complement activation or to eliminate granulocytes failed to kill the challenge larvae. Transfer of immune IgG into IL-5 knockout (KO) mice, which are deficient in eosinophils, resulted in larval attrition, while transfer into FcR␥ KO mice did not result in larval killing. These findings suggest that IgG from mice immunized with live L3 requires complement activation and neutrophils for killing of L3 through an antibody-dependent cellular cytotoxicity (ADCC) mechanism. This is in contrast to the results of investigations using IgM from mice immunized with live L3 and IgG from mice immunized with larval antigens soluble in deoxycholate in which protective immunity was shown to be ADCC independent. Western blot analyses with immune IgM and IgG identified few antigens recognized by all protective antibody isotypes. Results from immunoelectron microscopy demonstrated that the protective antibodies bound to different regions in the L3. It was therefore concluded that while IgM and IgG antibodies are both protective against larval S. stercoralis, they recognize different antigens and utilize different killing mechanisms.Large multicellular organisms like Strongyloides stercoralis present a significant challenge to the immune system, and the mechanisms by which this parasite is controlled and eliminated by the immune response remain poorly defined. In humans with severe strongyloidiasis, a significant decrease in the immunoglobulin M (IgM) and IgG levels was observed compared to the levels found in people with asymptomatic and mildly symptomatic infections. Eosinophil levels were also lower in people with severe strongyloidiasis than in individuals with asymptomatic or symptomatic infections. These findings suggest that antibody and eosinophils play a role in protective immunity to larval S. stercoralis in humans (5). In Erythrocebus patas monkeys and dogs infected with S. stercoralis, elevated anti-larval IgG titers were observed; however, it was not determined whether the elevated antibody titers were related to decreases in parasite survival (9, 12). Jirds can also support the complete S. stercoralis life cycle. It was determined that after a single primary infection, jirds eliminated the challenge infection within 24 h via a mechanism dependent on cell contact and a factor found in serum (27).To gain an understanding of how the immune response eliminates the larval stages of S. stercoralis, a mouse model was developed. In this model it was demonstrated that i...

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“…Eosinophils and antibodies participate in human immunity against S. stercoralis larvae and are likely to reduce the risk of developing severe forms of the disease because immunoglobulin levels and eosinophil numbers were significantly lower in patients with complicated disease than in patients with uncomplicated disease [24]. Additionally, the occurrence of both humoral and cellular responses, with increases in mast cell numbers and histamine levels in the host intestinal mucosa, was previously demonstrated in patas monkeys (Erythrocebus patas) infected with a human strain of S. stercoralis [25][26][27]. The mechanisms related to S. stercoralis dissemination in patients receiving corticosteroids are not yet fully known.…”

Section: Introductionmentioning

confidence: 97%

Strongyloides stercoralis infection in marmosets: replication of complicated and uncomplicated human disease and parasite biology

Mati

Raso²,

Melo

2014

Parasites & Vectors

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Both complicated and uncomplicated strongyloidiasis occur in C. penicillata that is described as a susceptible small non-human primate model for S. stercoralis. This host permits the maintenance of a human strain of the parasite in the laboratory and can be useful for experimental investigations of strongyloidiasis. In parallel, we discuss data related to the autoinfective cycle that provides new insights into the biology of S. stercoralis.

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Experimental Disseminated Strongyloidiasis in Erythrocebus patas

Cited by 26 publications

References 0 publications

L3 antigen‐specific antibody isotype responses in human strongyloidiasis: correlations with larval output

L3 antigen‐specific antibody isotype responses in human strongyloidiasis: correlations with larval output

Specificity and Mechanism of Immunoglobulin M (IgM)-and IgG-Dependent Protective Immunity to LarvalStrongyloides stercoralisinMice

Strongyloides stercoralis infection in marmosets: replication of complicated and uncomplicated human disease and parasite biology

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