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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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Photomicrographs of granulomas (A and B; hematoxylin and eosin staining) and fibrotic tissue (C and D; Gomori's trichrome staining) representative of the group means of animals neonatally injected with MSS Id (A and C) or HSS Id (B and D). Original magnification: ×200; bars, 50 μm.  Blue staining in C and D is indicative of fibrosis, some of which is periportal in HSS Id–injected animals (D).
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Figure 4: Photomicrographs of granulomas (A and B; hematoxylin and eosin staining) and fibrotic tissue (C and D; Gomori's trichrome staining) representative of the group means of animals neonatally injected with MSS Id (A and C) or HSS Id (B and D). Original magnification: ×200; bars, 50 μm. Blue staining in C and D is indicative of fibrosis, some of which is periportal in HSS Id–injected animals (D).

Mentions: We next analyzed the histopathological features of mice that were neonatally exposed to NoMoIgG, 8WkId, MSS Id, or HSS Id preparations and subsequently infected with S. mansoni. Mice that received 8WkId or MSS Id as newborns had a significantly smaller acute (8 wk) infection mean granuloma size (Fig. 3 A) and a significantly decreased percentage of fibrotic liver tissue at 8 wk after infection (Fig. 3 B) than mice that received NoMoIgG or HSS Id at birth. The histologic appearance of granulomas and fibrotic areas representative of these means is presented in Fig. 4. We also observed that mice receiving 8WkId or MSS Id at birth had decreased 8 wk–infection spleen to body weight ratios than animals neonatally injected with NoMoIgG or HSS Id (Table II). To determine whether these differences in pathology were simply an effect of differences in worm burdens, we measured CCA levels in these animals but found no significant difference between mice in any of the neonatal injection groups (Table II). However, in spite of the comparable worm burdens, mice that received HSS Id as newborns were found to have a significantly higher mean number of eggs per gram of liver than mice that had been injected with MSS Id (Table II), resulting in the fibrosis per egg between these two groups not being significantly different (data not shown). The numbers of eggs per gram of liver for mice neonatally injected with NoMoIgG or 8WkId were not significantly different from each other or from either the MSS Id or HSS Id injection groups (Table II).


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)

Photomicrographs of granulomas (A and B; hematoxylin and eosin staining) and fibrotic tissue (C and D; Gomori's trichrome staining) representative of the group means of animals neonatally injected with MSS Id (A and C) or HSS Id (B and D). Original magnification: ×200; bars, 50 μm.  Blue staining in C and D is indicative of fibrosis, some of which is periportal in HSS Id–injected animals (D).
© Copyright Policy
Related In: Results  -  Collection

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

Figure 4: Photomicrographs of granulomas (A and B; hematoxylin and eosin staining) and fibrotic tissue (C and D; Gomori's trichrome staining) representative of the group means of animals neonatally injected with MSS Id (A and C) or HSS Id (B and D). Original magnification: ×200; bars, 50 μm. Blue staining in C and D is indicative of fibrosis, some of which is periportal in HSS Id–injected animals (D).
Mentions: We next analyzed the histopathological features of mice that were neonatally exposed to NoMoIgG, 8WkId, MSS Id, or HSS Id preparations and subsequently infected with S. mansoni. Mice that received 8WkId or MSS Id as newborns had a significantly smaller acute (8 wk) infection mean granuloma size (Fig. 3 A) and a significantly decreased percentage of fibrotic liver tissue at 8 wk after infection (Fig. 3 B) than mice that received NoMoIgG or HSS Id at birth. The histologic appearance of granulomas and fibrotic areas representative of these means is presented in Fig. 4. We also observed that mice receiving 8WkId or MSS Id at birth had decreased 8 wk–infection spleen to body weight ratios than animals neonatally injected with NoMoIgG or HSS Id (Table II). To determine whether these differences in pathology were simply an effect of differences in worm burdens, we measured CCA levels in these animals but found no significant difference between mice in any of the neonatal injection groups (Table II). However, in spite of the comparable worm burdens, mice that received HSS Id as newborns were found to have a significantly higher mean number of eggs per gram of liver than mice that had been injected with MSS Id (Table II), resulting in the fibrosis per egg between these two groups not being significantly different (data not shown). The numbers of eggs per gram of liver for mice neonatally injected with NoMoIgG or 8WkId were not significantly different from each other or from either the MSS Id or HSS Id injection groups (Table II).

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