Strongyloides stercoralis: Protective Immunity to Third-Stage Larvae in BALB/cByJ Mice

Abraham, David; Rotman, Harris L.; Haberstroh, Hanna; Yutanawiboonchai, Wiboonchai; Brigandi, Richard A.; Leon, Ofra; Nolan, Thomas J.; Schad, Gerhard A.

doi:10.1006/expr.1995.1036

Cited by 79 publications

(86 citation statements)

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“…Protective immunity was shown to be dependent on IgM, from serum transfer experiments, and on complement activation, by depletion with cobra venom factor (26). Finally, depletion of granulocytes with the mAb RB6-8C5 eliminated protective immunity in immunized mice, which, combined with the dependency on IL-5, supported the hypothesis that eosinophils were required for larval killing by the adaptive immune response (27).…”

mentioning

confidence: 72%

“…stercoralis L3 were obtained from the fresh stools of a laboratory dog infected with the parasite according to methods previously described (27). Larvae were collected from charcoal cultures and washed by centrifugation and resuspension in sterile RPMI with 100 U/ml penicillin, 0.1 mg/ml streptomycin, and 0.1 mg/ml gentamicin (antibiotics) (Sigma, St. Louis, MO)…”

Section: Experimental Animals and Parasitesmentioning

confidence: 99%

“…Mice were immunized with live S. stercoralis L3 as described previously (27). The immunization protocol consisted of two s.c. injections with 5,000 live L3 administered 2 wk apart, followed by a challenge infection given 1 wk later consisting of 50 live L3 contained within diffusion chambers or 1000 live L3 injected s.c. Construction of diffusion chambers and challenge infection of mice with L3 followed previously published methods (27).…”

Section: Immunization and Challenge Infectionsmentioning

confidence: 99%

“…The immunization protocol consisted of two s.c. injections with 5,000 live L3 administered 2 wk apart, followed by a challenge infection given 1 wk later consisting of 50 live L3 contained within diffusion chambers or 1000 live L3 injected s.c. Construction of diffusion chambers and challenge infection of mice with L3 followed previously published methods (27). Fourteen-millimeter Lucite (Millipore, Bedford, MA) rings were covered with 2.0-m Isopore membranes (Millipore).…”

Section: Immunization and Challenge Infectionsmentioning

confidence: 99%

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Role of IL-5 in Innate and Adaptive Immunity to LarvalStrongyloides stercoralisin Mice

Herbert

Lee

et al. 2000

The Journal of Immunology

113

110

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Protective immunity to Strongyloides stercoralis infective larvae in mice has been shown to be dependent on IL-5 based on mAb depletion studies. The goal of this study was to determine the functional role of IL-5 during the innate and adaptive immune response to larval S. stercoralis in mice. In these studies, three strains of mice were used: wild-type C57BL/6J (WT), IL-5 knockout (KO), and IL-5 transgenic (TG). Innate responses to the larvae indicated that there was enhanced survival in the KO animals and decreased survival in the TG animals compared with WT. Furthermore, killing of larvae in TG mice was associated with eosinophil infiltration and degranulation. In studying the adaptive immune response, it was observed that immunization of KO mice did not lead to the development of protective immunity. Experiments were then performed to determine whether KO mice reconstituted with Abs or cells could then develop protective immunity. KO mice displayed protective immunity via a granulocyte-dependent mechanism following injection of purified IgM from immune wild-type animals. Immunity in KO mice could also be reconstituted by the injection of eosinophils at the time of immunization. These eosinophils did not participate in actively killing the challenge infection, but rather were responsible for the induction of a protective Ab response. We conclude that IL-5 is required in the protective immune response for the production of eosinophils, and that eosinophils were involved in larval killing during innate immunity and in the induction of protective Abs in the adaptive immune response.

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mentioning

confidence: 72%

Section: Experimental Animals and Parasitesmentioning

confidence: 99%

Section: Immunization and Challenge Infectionsmentioning

confidence: 99%

Section: Immunization and Challenge Infectionsmentioning

confidence: 99%

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Role of IL-5 in Innate and Adaptive Immunity to LarvalStrongyloides stercoralisin Mice

Herbert

Lee

et al. 2000

The Journal of Immunology

113

110

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“…3 The infection induces Th2 immune responses in humans (12,13), and protective immunity to L3 in humans operates through an Ab-dependent mechanism (14). In mice, the immune mechanisms capable of killing larval S. stercoralis have been studied on a variety of mouse backgrounds, including C57BL/6J, BALB/cJ, BALB/cByJ, and CBA/J (15)(16)(17). Innate protective immunity, evaluated 3 days after infection of naive mice, was shown to be IL-5 and eosinophil dependent (18).…”

mentioning

confidence: 99%

Complement Component C3 Is Required for Protective Innate and Adaptive Immunity to Larval Strongyloides stercoralis in Mice

Kerepesi

Hess

Nolan

et al. 2006

The Journal of Immunology

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This study examines the role of complement components C3 and C5 in innate and adaptive protective immunity to larval Strongyloides stercoralis in mice. Larval survival in naive C3−/− mice was increased as compared with survival in wild-type mice, whereas C3aR−/− and wild-type mice had equivalent levels of larval killing. Larval killing in naive mice was shown to be a coordinated effort between effector cells and C3. There was no difference between survival in wild-type and naive C5−/− mice, indicating that C5 was not required during the innate immune response. Naive B cell-deficient and wild-type mice killed larvae at comparable levels, suggesting that activation of the classical complement pathway was not required for innate immunity. Adaptive immunity was equivalent in wild-type and C5−/− mice; thus, C5 was also not required during the adaptive immune response. Larval killing was completely ablated in immunized C3−/− mice, even though the protective parasite-specific IgM response developed and effector cells were recruited. Protective immunity was restored to immunized C3−/− mice by transferring untreated naive serum, but not C3-depleted heat-inactivated serum to the location of the parasites. Finally, immunized C3aR−/− mice killed larvae during the adaptive immune response as efficiently as wild-type mice. Therefore, C3 was not required for the development of adaptive immunity, but was required for the larval killing process during both protective innate and adaptive immune responses in mice against larval S. stercoralis.

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Strongyloides stercoralis and Strongyloidosis

Korenaga

Bruschi

2022

Helminth Infections and Their Impact on Global Public Health

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Strongyloides stercoralis: Protective Immunity to Third-Stage Larvae in BALB/cByJ Mice

Cited by 79 publications

References 0 publications

Role of IL-5 in Innate and Adaptive Immunity to LarvalStrongyloides stercoralisin Mice

Role of IL-5 in Innate and Adaptive Immunity to LarvalStrongyloides stercoralisin Mice

Complement Component C3 Is Required for Protective Innate and Adaptive Immunity to Larval Strongyloides stercoralis in Mice

Strongyloides stercoralis and Strongyloidosis

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