Effects of environmentally relevant concentrations of 2,3,7,8-TCDD on domestic chicken immune function and CYP450 activity: F1 generation and EGG injection studies

Peden‐Adams, Margie M.; Alonso, K.; Godard, Céline A. J.; Skipper, Sherry L.; Mashburn, WE; Hoover, J.L.; Charbonneau, Collette S.; Henshe, D.; Dickerson, R.

doi:10.1016/s0045-6535(98)00259-8

Cited by 16 publications

(10 citation statements)

References 23 publications

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“…Naïve B cell cultures were prepared, as published elsewhere, in duplicate at 2×10 5 cell/ml with 0.5, 1, 5, or 10 μg/ml LPS (Sigma), 1, 5, or 10 μg/ml anti-IgM (Jackson ImmunoResearch), 10 ng/ml phorbol 12-myristate 13-acetate (PMA) (Sigma) and 0.25, 0.5, or 1 μg/ml ionomycin (Sigma), or 1, 5, or 10 μg/ml CpG oligonucleotides (Cell Sciences) [37, 38]. Cultures were incubated at 37°C in 5% CO 2 for 48 hours prior to addition of 5 μCi/ml tritiated thymidine and incubation at 37°C in 5% CO 2 for 14 hours [39].…”

Section: Methodsmentioning

confidence: 99%

A role for Fli-1 in B cell proliferation: Implications for SLE pathogenesis

Bradshaw

Zheng

Tsoi

et al. 2008

Clinical Immunology

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Transgenic overexpression of Fli-1 in normal mice leads to SLE-like disease and increased expression was reported in SLE-affected human and murine lymphocytes. Reducing Fli-1 expression in MRL/lpr mice decreased antibody production, proteinuria, renal pathology, and mortality. Compared to those with wild-type expression of Fli-1, we report here that proliferative responses of Fli-1-deficient naïve B cells to several mitogens were reduced in lupus-prone and control mice. Expression of mitogen receptors, including BCR, TLR4, and TLR9, was not significantly impacted in Fli-1-deficient naïve B cells. IL12a transcripts were upregulated and NFAT transcripts were downregulated in Fli-1-deficient MRL/lpr B cells. These results demonstrate that Fli-1 deficiency affects B cell proliferative responses to mitogens, independent of BCR and TLR expression. IL12a and NFAT, known to influence proliferation, were identified as potential mediators of this effect. This may be a mechanism by which overexpression of Fli-1 contributes to B cell hyperactivity and subsequent SLE pathogenesis.

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Section: Methodsmentioning

confidence: 99%

A role for Fli-1 in B cell proliferation: Implications for SLE pathogenesis

Bradshaw

Zheng

Tsoi

et al. 2008

Clinical Immunology

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“…TCDD (2, 3, 7, 8-tetrachlorodibenzo-p-dioxin) is an environmental pollutant, known to cause various types of toxicities, such as teratogenicity, immunotoxicity, and reproductive toxicity (Bird et al 1983;Larson et al 1995;Walker et al 1997;Peden-Adams et al 1998;Blankenship et al 2003). Cardiac abnormalities are one of the most severe teratogenicities in avian species.…”

Section: Introductionmentioning

confidence: 99%

TCDD-induced chick cardiotoxicity is abolished by a selective cyclooxygenase-2 (COX-2) inhibitor NS398

et al. 2014

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Halogenated aromatic hydrocarbons (HAHs), including 2, 3, 7,, are known to cause severe heart defects in avian species. However, the mechanism of TCDD-induced chick cardiovascular toxicity is unclear. In this study, we investigated cyclooxygenase-2 (COX-2) as a possible mechanism of TCDD-induced cardiotoxicity. Fertile chicken eggs were injected with TCDD and a COX-2 selective inhibitor, NS398, and we investigated chick heart failure on day 10. We found that the chick heart to body weight ratio and atrial natriuretic factor (ANF) mRNA expression were increased but this increase was abolished with treatment of NS398. In addition, the morphological abnormality of an enlarged ventricle resulting from TCDD exposure was also abolished with co-treatment of TCDD and NS398. Our results suggested that TCDD-induced chick heart defects are mediated via the nongenomic pathway and that they do not require the genomic pathway.

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“…The types of toxicity induced include teratogenic, immunotoxic and reproductive toxicity [1, 2, 19, 23, 31]. The dioxin concentration required to induce these types of toxicity varies significantly between birds [3].…”

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confidence: 99%

Dioxin Sensitivity-Related Two Critical Amino Acids of Arylhydrocarbon Receptor May Not Correlate with the Taxonomy or Phylogeny in Avian Species

Fujisawa

Kawai

Nakayama

et al. 2013

The Journal of Veterinary Medical Science

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There are two arylhydrocarbon receptor (AhR) isoforms in birds, AhR1 and AhR2. The varying sensitivity of AhR is reported to be related to two critical amino acids at positions 325 and 381 in the AhR1 ligand-binding domain. In this study, seven avian species whose in vivo dioxin sensitivity was known, and 13 species with no data regarding their in vivo dioxin sensitivity were examined. The two critical amino acids in the ligand-binding domain were investigated in avian species, and the results were compared with the taxonomy or phylogenetic trees for the bird AhR proteins. We found that the two critical amino acids did not correlate with the taxonomy or phylogeny of these proteins, suggesting that dioxin sensitivity was independent of taxonomy.

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Effects of environmentally relevant concentrations of 2,3,7,8-TCDD on domestic chicken immune function and CYP450 activity: F1 generation and EGG injection studies

Cited by 16 publications

References 23 publications

A role for Fli-1 in B cell proliferation: Implications for SLE pathogenesis

A role for Fli-1 in B cell proliferation: Implications for SLE pathogenesis

TCDD-induced chick cardiotoxicity is abolished by a selective cyclooxygenase-2 (COX-2) inhibitor NS398

Dioxin Sensitivity-Related Two Critical Amino Acids of Arylhydrocarbon Receptor May Not Correlate with the Taxonomy or Phylogeny in Avian Species

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