Mycotoxin T-2 and aflatoxin B1 asimmunosuppressors in mice chronically infected with Toxoplasma gondii

Venturini, Marı́a Cecilia; Quiroga, María Alejandra; Risso, Miguel Atilio; Lorenzo, C. Di; Omata, Yoshitaka; Venturini, L.; Godoy, Héctor M.

doi:10.1016/s0021-9975(96)80081-8

Cited by 42 publications

(14 citation statements)

References 15 publications

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“…El análisis histopatológico se realizó mediante procedimiento de rutina con la tinción con hematoxilina y eosina (H/E). Se evaluó la aparición y severidad de las lesiones histopatológicas según el siguiente esquema de puntuación (Pereira et al, 2017;Venturini et al, 1996):…”

Section: Análisis Histopatológicounclassified

Congenital human toxoplasmosis caused by non-clonal Toxoplasma gondii genotypes in Argentina

Pardini

Bernstein

Carral

et al. 2019

Parasitology International

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Section: Análisis Histopatológicounclassified

Congenital human toxoplasmosis caused by non-clonal Toxoplasma gondii genotypes in Argentina

Pardini

Bernstein

Carral

et al. 2019

Parasitology International

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“…Further, pathogen recognition is impaired in human leukocytes by AF treatment (Malvandi et al, 2013). Exposure of pigs to AF-contaminated feed increases their susceptibility to infection and reduces vaccine-induced protection, mainly through the dysregulation of T-cell polarization (Meissonnier et al, 2008;Venturini et al, 1996). This led to the assumption that AF interfere with the function of antigen-presenting cells, such as dendritic cells (DC), as these cells drive the polarization of naïve T-cells (Meissonnier et al, 2008).…”

Section: Introductionmentioning

confidence: 99%

Aflatoxins of type B and G affect porcine dendritic cell maturationin vitro

Mehrzad

Devriendt

Baert

et al. 2014

Journal of Immunotoxicology

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The toxic effects of highly carcinogenic mycotoxins, especially aflatoxins (AF), on key antigenpresenting cells, such as dendritic cells (DC), are largely unknown. To elucidate the effect of AF on DC function, porcine monocyte-derived DC (MoDC) were treated with a mixture of several AF (i.e., AFB 1 , AFB 2 , AFG 1 , and AFG 2 ) and the phagocytic capacity, the membrane expression level of several DC activation markers, the T-cell proliferation-inducing capacity, and the cytokine secretion pattern were assessed. As compared to untreated MoDC, AF significantly up-regulated the expression of the co-stimulatory molecules CD25 and CD80/86. However, the phagocytic activity of MoDC was not affected by AF treatment. While the cytokine secretion pattern of AF-treated MoDC was similar to control MoDC, the T-cell proliferation-inducing capacity of MoDC was increased upon aflatoxin treatment. The results indicate that a mixture of naturally occurring AF enhances the antigen-presenting capacity of DC, which could explain the observed immunotoxicity of AF by breaking down tolerance and further emphasizes the need to reduce the admissible level of AF in agricultural commodities.

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“…These types of intracellular insults alter the expression of genes important for cellular homeostasis as well as ones integral for a variety of pathogenic processes involved in cell survival, proliferation, and stress responses 51,52 . Depending on the underlying mechanism as well as exposure dose, duration, and frequency, toxic agents can cause immune suppression and cytotoxicity in various experimental animals that develop symptoms such as leucopenia and enhanced susceptibility to infection [53][54][55][56][57][58] .…”

Section: Introductionmentioning

confidence: 99%

Integrated stress response-altered pro-inflammatory signals in mucosal immune-related cells

Park

Moon

2012

Immunopharmacology and Immunotoxicology

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Various cells are associated with the integrated stress response (ISR) that leads to translation arrest via phosphorylation of the alpha subunit of eukaryotic translation initiation factor 2. Pathogenic insults or nutritional imbalance in the mucosal tissues including the intestinal, airway, and genitourinary epithelia can cause ISRs, which have been linked to different mucosal inflammatory responses and subsequent systemic diseases. In particular, translational arrest caused by the early recognition of luminal microbes as well as nutritional status allows the human body to mount appropriate responses and maintain homeostasis both at the cellular and systemic levels. However, an over- or reduced ISR can create pathogenic conditions such as inflammation and carcinogenesis. This present review explores the association between eIF2α kinase-linked pathways and mucosal or systemic pro-inflammatory signals activated by xenobiotic insults (such as ones caused by microbes or nutritional abnormalities). Understanding ISR-modulated cellular alterations will provide progressive insights into approaches for treating human mucosal inflammatory and metabolic disorders.

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Mycotoxin T-2 and aflatoxin B1 asimmunosuppressors in mice chronically infected with Toxoplasma gondii

Cited by 42 publications

References 15 publications

Congenital human toxoplasmosis caused by non-clonal Toxoplasma gondii genotypes in Argentina

Congenital human toxoplasmosis caused by non-clonal Toxoplasma gondii genotypes in Argentina

Aflatoxins of type B and G affect porcine dendritic cell maturationin vitro

Integrated stress response-altered pro-inflammatory signals in mucosal immune-related cells

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