Analysis Tools
mortality/aging
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• over 80% of mice survive infection with S. mansoni compared to 50% of wild-type mice
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immune system
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• following infection with S. mansoni, mice exhibit a modestly higher frequency of eosinophils in granulomatous lesions compared to wild-type mice
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• the number of interferon-gamma producing CD4+ T cells increases at 12 weeks of age
• 12 days after infection with N. resiliencies, mice produce more IL-5 and IL-3 producing CD4+ T cell
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• mice acutely and chronically infected with S. mansoni exhibit increased Th2 CD4+ T cells in the liver compared to wild-type mice
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• 8 weeks following infection with S. mansoni, mice exhibit increased IgA levels compared to in wild-type mice
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• mice chronically infected with S. mansoni exhibit decreased IgE levels compared to wild-type mice
• mice exposed to intratracheal S. mansoni egg antigen exhibit lower IgE levels than in wild-type mice
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• 8 weeks following infection with S. mansoni, mice exhibit increased IgG1 levels compared to in wild-type mice
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• 8 weeks following infection with S. mansoni, mice exhibit increased IgG3 levels compared to in wild-type mice
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• Th2 response is enhanced compared to wild-type mice following infection with S. mansoni or N. brasiliensis and exposure to intratracheal S. mansoni egg antigen
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• IL-5 production is increased during S. mansoni infection compared to in wild-type mice
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• despite increased Th2 response mice are unable to clear N. brasiliensis
• when challenged intratracheally with S. mansoni egg antigen mice exhibit an enhanced Th2 response with fewer eosinophil and more macrophage infiltration into the lungs
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• mice exhibit less hepatic fibrosis than in wild-type mice in response to infection with S. mansoni
• over 80% of mice survive infection with S. mansoni compared to 50% of wild-type mice
• chronically infected mice exhibit lowered serum levels of alanine aminotransferase, aspartate aminotransferase and alkaline phosphatase compared to wild-type mice infected with S. mansoni indicating reduced liver damage and biliary obstruction
• however, parasitic burden is the same as in wild-type mice when infected with S. mansoni
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homeostasis/metabolism
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• IL-5 production is increased during S. mansoni infection compared to in wild-type mice
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• unlike in wild-type mice, interferon-gamma-induced nitric oxide is not inhibited by IL-3
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respiratory system
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• mice exhibit decreased airway hyperreactivity in response to intratracheal administration of S. mansoni egg antigen compared to wild-type mice
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hematopoietic system
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• following infection with S. mansoni, mice exhibit a modestly higher frequency of eosinophils in granulomatous lesions compared to wild-type mice
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• the number of interferon-gamma producing CD4+ T cells increases at 12 weeks of age
• 12 days after infection with N. resiliencies, mice produce more IL-5 and IL-3 producing CD4+ T cell
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• mice acutely and chronically infected with S. mansoni exhibit increased Th2 CD4+ T cells in the liver compared to wild-type mice
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• 8 weeks following infection with S. mansoni, mice exhibit increased IgA levels compared to in wild-type mice
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• mice chronically infected with S. mansoni exhibit decreased IgE levels compared to wild-type mice
• mice exposed to intratracheal S. mansoni egg antigen exhibit lower IgE levels than in wild-type mice
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• 8 weeks following infection with S. mansoni, mice exhibit increased IgG1 levels compared to in wild-type mice
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• 8 weeks following infection with S. mansoni, mice exhibit increased IgG3 levels compared to in wild-type mice
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• Th2 response is enhanced compared to wild-type mice following infection with S. mansoni or N. brasiliensis and exposure to intratracheal S. mansoni egg antigen
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