Celiac Disease Increases the Risk of Toxoplasma gondii Infection in a Large Cohort of Pregnant Women

Rostami‐Nejad, Mohammad; Rostami, Kamran; Cheraghipour, Kourosh; Nazemalhosseini‐Mojarad, Ehsan; Volta, Umberto; Dulaimi, David Al; Zali, Mohammad Reza

doi:10.1038/ajg.2010.425

Cited by 16 publications

(11 citation statements)

References 3 publications

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“…This reasoning is strongly supported by the recent report of Severance et al [848] that in mice receiving a standard wheat-based rodent chow, peroral, intraperitoneal and prenatal T. gondii exposure launched a highly significant generation of anti-gluten IgG antibodies in all infected animals compared to uninfected controls (P ≤ 0.00001). Perorally-infected females showed higher concentrations of anti-gluten IgG than males (P ≤ 0.009) indicating that the parasite-generated gastrointestinal infection led to a marked anti-gluten response in a sex-dependent manner [848]. These findings may be explained by the facts that: 1) transepithelial migration of T. gondii is linked to its active motility and virulence [849], 2) involves an interaction of human ICAM-1 with the parasite adhesin MIC2 resulting in its immunoprecipitation [317], and 3) the parasite targets the paracellular pathway to invade the intestinal epithelium and affects epithelial tight junction-associated proteins [10], thus finally affecting host intestinal wall permeability.…”

Section: Possible Association Between T1dm Celiac Disease (Cd) and Tsupporting

confidence: 73%

“…Critical analysis of the literature data suggests however that on the contrary, chronic latent infection with the parasite increases the risk of celiac disease development [809]. This reasoning is strongly supported by the recent report of Severance et al [848] that in mice receiving a standard wheat-based rodent chow, peroral, intraperitoneal and prenatal T. gondii exposure launched a highly significant generation of anti-gluten IgG antibodies in all infected animals compared to uninfected controls (P ≤ 0.00001). Perorally-infected females showed higher concentrations of anti-gluten IgG than males (P ≤ 0.009) indicating that the parasite-generated gastrointestinal infection led to a marked anti-gluten response in a sex-dependent manner [848].…”

Section: Possible Association Between T1dm Celiac Disease (Cd) and Tsupporting

confidence: 70%

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T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Pr¹,

ota²

2013

J Diabetes Metab

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Recently, it was suggested that maternal T and potentially B cells transferred during pregnancy and/or the breast milk feeding and their encounter with the antigen in mesenteric lymph nodes might play a role in development of type 1 diabetes mellitus (T1DM). T. gondii infection during gestation and/or after birth may be responsible for development of both T1DM and T2DM in children, adolescents and adults because: a) maternal microchimerism in peripheral blood was demonstrated to be significantly higher in patients with T1DM compared to unaffected siblings and healthy subjects, b) transmission of T. gondii as a Trojan horse in various types of eukaryotic cells, including T and B lymphocytes, c) swallowing by the fetus of amniotic fluid containing infected leukocytes and other cells, d) elimination of T. gondii in the breast milk during lactation, e) involvement of mesenteric lymph nodes after oral infection with the parasite, and f) damage of the myenteric neurons during infection with the parasite in both the animals with streptozotocin-induced diabetes and diabetic patients. Moreover, a significantly lower occurrence of antibodies against T. gondii found in the sera of patients with T1DM compared with their first-degree family members or healthy controls may be due to their T and/or B cell exhaustion perspective caused by chronic infection with the parasite. This suggestion may be supported by the finding that latent toxoplasmosis was associated with markedly reduced lymphocyte B-cell counts responsible for production of antibodies, markedly lower serum IgG, IgM, and IgA levels, and a significant suppression of IL-2. On the other hand, patients with T2DM had increased anti-T. gondii antibodies significantly more frequently than respective controls. Impaired vascular endothelial function characteristic for the patients with diabetes mellitus may be at least in part due to the preferential T. gondii infection of endothelial cells. Vitamin D and minocycline exerted beneficial effects on development and clinical course of diabetes mellitus probably because of their immunomodulatory and antitoxoplasmatic activities. These data strongly suggest that the parasite play an important role in development of both types of diabetes mellitus.

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Section: Possible Association Between T1dm Celiac Disease (Cd) and Tsupporting

confidence: 73%

Section: Possible Association Between T1dm Celiac Disease (Cd) and Tsupporting

confidence: 70%

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Pr¹,

ota²

2013

J Diabetes Metab

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show abstract

“…These findings were supported by a mouse model of peroral T. gondii infection where infected animals had elevated antibody levels to dietary gluten compared to those that were uninfected (Severance et al, 2012c). Links between measures of T. gondii exposure and celiac disease have also been reported, although it was not possible to determine if infection or the enteropathic state came first (Lidar et al, 2009; Rostami Nejad et al, 2011). Additional studies have documented that T. gondii infection impacts the resident microbiota communities and brings about a state of inflammation conducive to the process of bacterial translocation, a surrogate measure of GI permeability (Craven et al, 2012; Grainger et al, 2013; Hand et al, 2012; Heimesaat et al, 2006).…”

Section: Extra-autoimmune Gi Connection To Schizophreniamentioning

confidence: 99%

Autoimmune diseases, gastrointestinal disorders and the microbiome in schizophrenia: more than a gut feeling

Severance¹,

Yolken²,

Eaton

2016

Schizophrenia Research

210

149

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Autoimmunity, gastrointestinal (GI) disorders and schizophrenia have been associated with one another for a long time. This paper reviews these connections and provides a context by which multiple risk factors for schizophrenia may be related. Epidemiological studies strongly link schizophrenia with autoimmune disorders including enteropathic celiac disease. Exposure to wheat gluten and bovine milk casein also contribute to non-celiac food sensitivities in susceptible individuals. Co-morbid GI inflammation accompanies humoral immunity to food antigens, occurs early during the course of schizophrenia and appears to be independent from antipsychotic-generated motility effects. This inflammation impacts endothelial barrier permeability and can precipitate translocation of gut bacteria into systemic circulation. Infection by the neurotropic gut pathogen, Toxoplasma gondii, will elicit an inflammatory GI environment. Such processes trigger innate immunity, including activation of complement C1q, which also functions at synapses in the brain. The emerging field of microbiome research lies at the center of these interactions with evidence that the abundance and diversity of resident gut microbiota contribute to digestion, inflammation, gut permeability and behavior. Dietary modifications of core bacterial compositions may explain inefficient gluten digestion and how immigrant status in certain situations is a risk factor for schizophrenia. Gut microbiome research in schizophrenia is in its infancy, but data in related fields suggest disease-associated altered phylogenetic compositions. In summary, this review surveys associative and experimental data linking autoimmunity, GI activity and schizophrenia, and proposes that understanding of disrupted biological pathways outside of the brain can lend valuable information regarding pathogeneses of complex, polygenic brain disorders.

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“…In humans, increased titers of T. gondii antibodies have been found in individuals with inflammatory bowel disease and celiac disease [35]. In pregnant women, T. gondii infection rates were higher among those with celiac disease compared to those without a gluten sensitivity [36]. It is not possible to discern from these studies if GI pathologies preceded T. gondii infection or vice versa.…”

Section: Introductionmentioning

confidence: 99%

Anti-Gluten Immune Response following Toxoplasma gondii Infection in Mice

et al. 2012

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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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Celiac Disease Increases the Risk of Toxoplasma gondii Infection in a Large Cohort of Pregnant Women

Cited by 16 publications

References 3 publications

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

T. gondii Infection Acquired during Pregnancy and/or after Birth may be Responsible for Development of both Type 1 and 2 Diabetes Mellitus

Autoimmune diseases, gastrointestinal disorders and the microbiome in schizophrenia: more than a gut feeling

Anti-Gluten Immune Response following Toxoplasma gondii Infection in Mice

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