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Neonatal idiotypic exposure alters subsequent cytokine, pathology, and survival patterns in experimental Schistosoma mansoni infections.

Montesano MA, Colley DG, Eloi-Santos S, Freeman GL, Secor WE - J. Exp. Med. (1999)

Bottom Line: We have used an experimental murine system to address the role of Ids in this immunoregulation.Sera from mice with 8-wk Schistosoma mansoni infection, chronic (20-wk infection) moderate splenomegaly syndrome (MSS), or chronic hypersplenomegaly syndrome (HSS) were passed over an S. mansoni soluble egg antigen (SEA) immunoaffinity column to prepare Ids (8WkId, MSS Id, HSS Id).Furthermore, neonatal exposure to 8WkId or MSS Id, but not NoMoIgG or HSS Id, led to significantly smaller granuloma size and lower hepatic fibrosis levels in infected mice.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Microbiologia, Immunologia e Parasitologia, Universidade Federal de Juiz de Fora, Juiz de Fora, Minas Gerais, Brazil 36036.

ABSTRACT
Exposure to maternal idiotypes (Ids) or antigens might predispose a child to develop an immunoregulated, asymptomatic clinical presentation of schistosomiasis. We have used an experimental murine system to address the role of Ids in this immunoregulation. Sera from mice with 8-wk Schistosoma mansoni infection, chronic (20-wk infection) moderate splenomegaly syndrome (MSS), or chronic hypersplenomegaly syndrome (HSS) were passed over an S. mansoni soluble egg antigen (SEA) immunoaffinity column to prepare Ids (8WkId, MSS Id, HSS Id). Newborn mice were injected with 8WkId, MSS Id, HSS Id, or normal mouse immunoglobulin (NoMoIgG) and infected with S. mansoni 8 wk later. Mice exposed to 8WkId or MSS Id as newborns had prolonged survival and decreased morbidity compared with mice that received HSS Id or NoMoIgG. When stimulated with SEA, 8WkId, or MSS Id, spleen cells from mice neonatally injected with 8WkId or MSS Id produced more interferon gamma than spleen cells from mice neonatally injected with HSS Id or NoMoIgG. Furthermore, neonatal exposure to 8WkId or MSS Id, but not NoMoIgG or HSS Id, led to significantly smaller granuloma size and lower hepatic fibrosis levels in infected mice. Together, these results indicate that perinatal exposure to appropriate anti-SEA Ids induces long-term effects on survival, pathology, and immune response patterns in mice subsequently infected with S. mansoni.

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Neonatal exposure to 8WkId or MSS Id induces enhanced  IFN-γ production during subsequent infection. Newborn mice (<24 h  old) were injected with 50 μg of NoMoIgG, 8WkId, MSS Id, or HSS Id.  At 8 wk of age, animals were infected with S. mansoni. At 8 wk after infection, spleen cells were harvested and stimulated with SEA (4 μg/ml),  8WkId (40 μg/ml), MSS Id (40 μg/ml), or HSS Id (40 μg/ml). Data  represent means of IFN-γ levels in 48-h supernatants minus unstimulated  control values. The n values listed in the key indicate the number of mice  per group. Spleen cells from animals neonatally injected with 8WkId or  MSS Id produced significantly higher levels of IFN-γ (*P < 0.01) than  infected animals receiving NoMoIgG or HSS Id at birth when later stimulated with SEA, 8WkId, or MSS Id.
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Figure 5: Neonatal exposure to 8WkId or MSS Id induces enhanced IFN-γ production during subsequent infection. Newborn mice (<24 h old) were injected with 50 μg of NoMoIgG, 8WkId, MSS Id, or HSS Id. At 8 wk of age, animals were infected with S. mansoni. At 8 wk after infection, spleen cells were harvested and stimulated with SEA (4 μg/ml), 8WkId (40 μg/ml), MSS Id (40 μg/ml), or HSS Id (40 μg/ml). Data represent means of IFN-γ levels in 48-h supernatants minus unstimulated control values. The n values listed in the key indicate the number of mice per group. Spleen cells from animals neonatally injected with 8WkId or MSS Id produced significantly higher levels of IFN-γ (*P < 0.01) than infected animals receiving NoMoIgG or HSS Id at birth when later stimulated with SEA, 8WkId, or MSS Id.

Mentions: To study whether neonatal exposure to Id has an effect on cytokine profiles expressed in response to SEA or Id (11) during subsequent S. mansoni infections, spleen cells were harvested from 8 wk–infected mice that had been exposed to the different Id preparations 16 wk previously, as newborns. The spleen cells were stimulated with SEA or Id preparations, and the supernatants were assayed for cytokines. Spleen cells from mice infected for 8 wk that had received 8WkId or MSS Id as newborns produced higher levels of IFN-γ in response to SEA or stimulatory Id preparations (8WkId or MSS Id) than did spleen cells from mice neonatally exposed to NoMoIgG or HSS Id (Fig. 5). Consistent with previous results (11), and similar to anti-SEA Id preparations from hepatosplenic patients (2), HSS Id was not stimulatory for any of the measured responses for cells from any treatment group.


Neonatal idiotypic exposure alters subsequent cytokine, pathology, and survival patterns in experimental Schistosoma mansoni infections.

Montesano MA, Colley DG, Eloi-Santos S, Freeman GL, Secor WE - J. Exp. Med. (1999)

Neonatal exposure to 8WkId or MSS Id induces enhanced  IFN-γ production during subsequent infection. Newborn mice (<24 h  old) were injected with 50 μg of NoMoIgG, 8WkId, MSS Id, or HSS Id.  At 8 wk of age, animals were infected with S. mansoni. At 8 wk after infection, spleen cells were harvested and stimulated with SEA (4 μg/ml),  8WkId (40 μg/ml), MSS Id (40 μg/ml), or HSS Id (40 μg/ml). Data  represent means of IFN-γ levels in 48-h supernatants minus unstimulated  control values. The n values listed in the key indicate the number of mice  per group. Spleen cells from animals neonatally injected with 8WkId or  MSS Id produced significantly higher levels of IFN-γ (*P < 0.01) than  infected animals receiving NoMoIgG or HSS Id at birth when later stimulated with SEA, 8WkId, or MSS Id.
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Related In: Results  -  Collection

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getmorefigures.php?uid=PMC2192931&req=5

Figure 5: Neonatal exposure to 8WkId or MSS Id induces enhanced IFN-γ production during subsequent infection. Newborn mice (<24 h old) were injected with 50 μg of NoMoIgG, 8WkId, MSS Id, or HSS Id. At 8 wk of age, animals were infected with S. mansoni. At 8 wk after infection, spleen cells were harvested and stimulated with SEA (4 μg/ml), 8WkId (40 μg/ml), MSS Id (40 μg/ml), or HSS Id (40 μg/ml). Data represent means of IFN-γ levels in 48-h supernatants minus unstimulated control values. The n values listed in the key indicate the number of mice per group. Spleen cells from animals neonatally injected with 8WkId or MSS Id produced significantly higher levels of IFN-γ (*P < 0.01) than infected animals receiving NoMoIgG or HSS Id at birth when later stimulated with SEA, 8WkId, or MSS Id.
Mentions: To study whether neonatal exposure to Id has an effect on cytokine profiles expressed in response to SEA or Id (11) during subsequent S. mansoni infections, spleen cells were harvested from 8 wk–infected mice that had been exposed to the different Id preparations 16 wk previously, as newborns. The spleen cells were stimulated with SEA or Id preparations, and the supernatants were assayed for cytokines. Spleen cells from mice infected for 8 wk that had received 8WkId or MSS Id as newborns produced higher levels of IFN-γ in response to SEA or stimulatory Id preparations (8WkId or MSS Id) than did spleen cells from mice neonatally exposed to NoMoIgG or HSS Id (Fig. 5). Consistent with previous results (11), and similar to anti-SEA Id preparations from hepatosplenic patients (2), HSS Id was not stimulatory for any of the measured responses for cells from any treatment group.

Bottom Line: We have used an experimental murine system to address the role of Ids in this immunoregulation.Sera from mice with 8-wk Schistosoma mansoni infection, chronic (20-wk infection) moderate splenomegaly syndrome (MSS), or chronic hypersplenomegaly syndrome (HSS) were passed over an S. mansoni soluble egg antigen (SEA) immunoaffinity column to prepare Ids (8WkId, MSS Id, HSS Id).Furthermore, neonatal exposure to 8WkId or MSS Id, but not NoMoIgG or HSS Id, led to significantly smaller granuloma size and lower hepatic fibrosis levels in infected mice.

View Article: PubMed Central - PubMed

Affiliation: Departamento de Microbiologia, Immunologia e Parasitologia, Universidade Federal de Juiz de Fora, Juiz de Fora, Minas Gerais, Brazil 36036.

ABSTRACT
Exposure to maternal idiotypes (Ids) or antigens might predispose a child to develop an immunoregulated, asymptomatic clinical presentation of schistosomiasis. We have used an experimental murine system to address the role of Ids in this immunoregulation. Sera from mice with 8-wk Schistosoma mansoni infection, chronic (20-wk infection) moderate splenomegaly syndrome (MSS), or chronic hypersplenomegaly syndrome (HSS) were passed over an S. mansoni soluble egg antigen (SEA) immunoaffinity column to prepare Ids (8WkId, MSS Id, HSS Id). Newborn mice were injected with 8WkId, MSS Id, HSS Id, or normal mouse immunoglobulin (NoMoIgG) and infected with S. mansoni 8 wk later. Mice exposed to 8WkId or MSS Id as newborns had prolonged survival and decreased morbidity compared with mice that received HSS Id or NoMoIgG. When stimulated with SEA, 8WkId, or MSS Id, spleen cells from mice neonatally injected with 8WkId or MSS Id produced more interferon gamma than spleen cells from mice neonatally injected with HSS Id or NoMoIgG. Furthermore, neonatal exposure to 8WkId or MSS Id, but not NoMoIgG or HSS Id, led to significantly smaller granuloma size and lower hepatic fibrosis levels in infected mice. Together, these results indicate that perinatal exposure to appropriate anti-SEA Ids induces long-term effects on survival, pathology, and immune response patterns in mice subsequently infected with S. mansoni.

Show MeSH
Related in: MedlinePlus