Anti-gluten immune response following Toxoplasma gondii infection in mice.
Gluten sensitivity may affect disease pathogenesis in a subset of individuals who have schizophrenia, bipolar disorder or autism. Exposure to Toxoplasma gondii is a known risk factor for the development of schizophrenia, presumably through a direct pathological effect of the parasite on brain and be...
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Public Library of Science (PLoS)
2012-01-01
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Series: | PLoS ONE |
Online Access: | http://europepmc.org/articles/PMC3510169?pdf=render |
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author | Emily G Severance Geetha Kannan Kristin L Gressitt Jianchun Xiao Armin Alaedini Mikhail V Pletnikov Robert H Yolken |
author_facet | Emily G Severance Geetha Kannan Kristin L Gressitt Jianchun Xiao Armin Alaedini Mikhail V Pletnikov Robert H Yolken |
author_sort | Emily G Severance |
collection | DOAJ |
description | Gluten sensitivity may affect disease pathogenesis in a subset of individuals who have schizophrenia, bipolar disorder or autism. Exposure to Toxoplasma gondii is a known risk factor for the development of schizophrenia, presumably through a direct pathological effect of the parasite on brain and behavior. A co-association of antibodies to wheat gluten and to T. gondii in individuals with schizophrenia was recently uncovered, suggesting a coordinated gastrointestinal means by which T. gondii and dietary gluten might generate an immune response. Here, we evaluated the connection between these infectious- and food-based antigens in mouse models. BALB/c mice receiving a standard wheat-based rodent chow were infected with T. gondii via intraperitoneal, peroral and prenatal exposure methods. Significant increases in the levels of anti-gluten IgG were documented in all infected mice and in offspring from chronically infected dams compared to uninfected controls (repetitive measures ANOVAs, two-tailed t-tests, all p≤0.00001). Activation of the complement system accompanied this immune response (p≤0.002-0.00001). Perorally-infected females showed higher levels of anti-gluten IgG than males (p≤0.009) indicating that T. gondii-generated gastrointestinal infection led to a significant anti-gluten immune response in a sex-dependent manner. These findings support a gastrointestinal basis by which two risk factors for schizophrenia, T. gondii infection and sensitivity to dietary gluten, might be connected to produce the immune activation that is becoming an increasingly recognized pathology of psychiatric disorders. |
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language | English |
last_indexed | 2024-04-13T17:43:55Z |
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publisher | Public Library of Science (PLoS) |
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spelling | doaj.art-0d0f0265ef924e6799206424ff73aabe2022-12-22T02:37:03ZengPublic Library of Science (PLoS)PLoS ONE1932-62032012-01-01711e5099110.1371/journal.pone.0050991Anti-gluten immune response following Toxoplasma gondii infection in mice.Emily G SeveranceGeetha KannanKristin L GressittJianchun XiaoArmin AlaediniMikhail V PletnikovRobert H YolkenGluten sensitivity may affect disease pathogenesis in a subset of individuals who have schizophrenia, bipolar disorder or autism. Exposure to Toxoplasma gondii is a known risk factor for the development of schizophrenia, presumably through a direct pathological effect of the parasite on brain and behavior. A co-association of antibodies to wheat gluten and to T. gondii in individuals with schizophrenia was recently uncovered, suggesting a coordinated gastrointestinal means by which T. gondii and dietary gluten might generate an immune response. Here, we evaluated the connection between these infectious- and food-based antigens in mouse models. BALB/c mice receiving a standard wheat-based rodent chow were infected with T. gondii via intraperitoneal, peroral and prenatal exposure methods. Significant increases in the levels of anti-gluten IgG were documented in all infected mice and in offspring from chronically infected dams compared to uninfected controls (repetitive measures ANOVAs, two-tailed t-tests, all p≤0.00001). Activation of the complement system accompanied this immune response (p≤0.002-0.00001). Perorally-infected females showed higher levels of anti-gluten IgG than males (p≤0.009) indicating that T. gondii-generated gastrointestinal infection led to a significant anti-gluten immune response in a sex-dependent manner. These findings support a gastrointestinal basis by which two risk factors for schizophrenia, T. gondii infection and sensitivity to dietary gluten, might be connected to produce the immune activation that is becoming an increasingly recognized pathology of psychiatric disorders.http://europepmc.org/articles/PMC3510169?pdf=render |
spellingShingle | Emily G Severance Geetha Kannan Kristin L Gressitt Jianchun Xiao Armin Alaedini Mikhail V Pletnikov Robert H Yolken Anti-gluten immune response following Toxoplasma gondii infection in mice. PLoS ONE |
title | Anti-gluten immune response following Toxoplasma gondii infection in mice. |
title_full | Anti-gluten immune response following Toxoplasma gondii infection in mice. |
title_fullStr | Anti-gluten immune response following Toxoplasma gondii infection in mice. |
title_full_unstemmed | Anti-gluten immune response following Toxoplasma gondii infection in mice. |
title_short | Anti-gluten immune response following Toxoplasma gondii infection in mice. |
title_sort | anti gluten immune response following toxoplasma gondii infection in mice |
url | http://europepmc.org/articles/PMC3510169?pdf=render |
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