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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 injection of mice with a CRI-expressing human  mAb (E5) confers increased survival upon subsequent S. mansoni infection. Mice neonatally injected with E5 or NoHuIgG were infected at 8 wk  of age and monitored for survival over the next 20 wk of infection. The  neonatal injection is indicated in the key, and the initial number of mice  is shown in parentheses.
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Figure 2: Neonatal injection of mice with a CRI-expressing human mAb (E5) confers increased survival upon subsequent S. mansoni infection. Mice neonatally injected with E5 or NoHuIgG were infected at 8 wk of age and monitored for survival over the next 20 wk of infection. The neonatal injection is indicated in the key, and the initial number of mice is shown in parentheses.

Mentions: Although 8WkId, MSS Id, and HSS Id were all prepared on the same SEA-Sepharose column, we also tested survival of S. mansoni–infected mice injected neonatally with an mAb (E5) to counter the possibility that the effects observed in the survival studies were a consequence of SEA that had leached off the affinity column into the Id preparations. E5 was produced from a human heterohybridoma that shares CRIs with 8WkId and MSS Id (9, 12, 17). Because this Ab was not passed over the SEA affinity column, there is no chance that the preparation was contaminated with SEA. As with the polyclonal 8WkId or MSS Id preparations, neonatal exposure to E5 resulted in longer survival times than for mice that received NoHuIgG (Fig. 2).


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 injection of mice with a CRI-expressing human  mAb (E5) confers increased survival upon subsequent S. mansoni infection. Mice neonatally injected with E5 or NoHuIgG were infected at 8 wk  of age and monitored for survival over the next 20 wk of infection. The  neonatal injection is indicated in the key, and the initial number of mice  is shown in parentheses.
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2192931&req=5

Figure 2: Neonatal injection of mice with a CRI-expressing human mAb (E5) confers increased survival upon subsequent S. mansoni infection. Mice neonatally injected with E5 or NoHuIgG were infected at 8 wk of age and monitored for survival over the next 20 wk of infection. The neonatal injection is indicated in the key, and the initial number of mice is shown in parentheses.
Mentions: Although 8WkId, MSS Id, and HSS Id were all prepared on the same SEA-Sepharose column, we also tested survival of S. mansoni–infected mice injected neonatally with an mAb (E5) to counter the possibility that the effects observed in the survival studies were a consequence of SEA that had leached off the affinity column into the Id preparations. E5 was produced from a human heterohybridoma that shares CRIs with 8WkId and MSS Id (9, 12, 17). Because this Ab was not passed over the SEA affinity column, there is no chance that the preparation was contaminated with SEA. As with the polyclonal 8WkId or MSS Id preparations, neonatal exposure to E5 resulted in longer survival times than for mice that received NoHuIgG (Fig. 2).

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