Intracellular adhesion molecule-1 up-regulation on thyrocytes by iodine of non-obese diabetic.H2h4 mice is reactive oxygen species-dependent

Sharma, Rajni; Traore, Kassim; Trush, Michael A.; Nr, Rose; Burek, C. Lynne

doi:10.1111/j.1365-2249.2008.03590.x

Cited by 37 publications

(31 citation statements)

References 36 publications

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“…A way to explain the toxicity of OS in thyroiditis in NOD mice is the induction of intracellular adhesion molecule-1 by ROS. 46 In the presence of NAC, the intracellular ROS production and OS were significantly reduced both in vitro and in vivo. As precursor of glutathione, NAC may decrease cell OS directly or indirectly by restoring glutathione content.…”

Section: Discussionmentioning

confidence: 96%

N-Acetylcysteine and 15 Deoxy-Δ12,14-Prostaglandin J2 Exert a Protective Effect Against Autoimmune Thyroid Destruction in Vivo but Not Against Interleukin-1α/Interferon γ-Induced Inhibitory Effects in Thyrocytes in Vitro

Poncin

Colin

Decallonne

et al. 2010

The American Journal of Pathology

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Reactive oxygen species (ROS) are crucial for thyroid hormonogenesis, and their production is kept under tight control. Oxidative stress (OS) is toxic for thyrocytes in an inflammatory context. In vitro, Th1 proinflammatory cytokines have already been shown to decrease thyroid-specific protein expression. In the present study, OS level and its impact on thyroid function were analyzed in vitro in Th1 cytokine (interleukin [IL]-1␣/interferon [IFN] ␥)-incubated thyrocytes (rat and human), as well as in vivo in thyroids from nonobese diabetic mice, a model of spontaneous autoimmune thyroiditis. N-acetylcysteine (NAC) and prostaglandin, 15 deoxy-⌬12 ,14 -prostaglandinJ2 (15dPGJ2), were used for their antioxidant and antiinflammatory properties, respectively. ROS production and OS were increased in IL-1␣/IFN␥-incubated thyrocytes and in destructive thyroiditis. In vitro, NAC not only reduced ROS production below control levels, but further decreased the expression of thyroid-specific proteins in addition to IL-1␣/IFN␥-inhibitory effects. Thus, besides ROS, other intracellular intermediaries likely mediate Th1 cytokine effects. In vivo, NAC and 15dPGJ2 reduced OS and the immune infiltration, thereby leading to a restoration of thyroid morphology. It is therefore likely that NAC and 15dPGJ2 mainly exert their protective effects by acting on infiltrating inflammatory cells rather than directly on thyrocytes.

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Section: Discussionmentioning

confidence: 96%

N-Acetylcysteine and 15 Deoxy-Δ12,14-Prostaglandin J2 Exert a Protective Effect Against Autoimmune Thyroid Destruction in Vivo but Not Against Interleukin-1α/Interferon γ-Induced Inhibitory Effects in Thyrocytes in Vitro

Poncin

Colin

Decallonne

et al. 2010

The American Journal of Pathology

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“…This process has been postulated to operate via the elevated generation of reactive oxygen intermediates. 35,37 However, the same dietary regimen does not appear to cause overt histological changes in the thyrocytes of other mouse strains -except for SJL 18 -and the genetic factors predisposing NOD. H2 h4 mice to ISAT remain unknown.…”

Section: Discussionmentioning

confidence: 99%

Iodine content of thyroglobulin in NOD.H2h4 mice developing iodine-accelerated autoimmune thyroiditis

Kolypetri

Noel

Carayanniotis

et al. 2010

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oBJective: In NOD.H2 h4 mice, high dietary iodine intake has been known to cause Iodineaccelerated spontaneous Autoimmune thyroiditis (IsAt) via an unknown mechanism. the aim of the study was to examine whether the NOD.H2 h4 genetic background predisposes to enhanced iodine organification in thyroglobulin (tg), a target autoantigen in IsAt. DEsIGN: to avoid issues associated with an ongoing anti-tg antibody response, we assessed tg iodination levels in iodine-fed, b-cell deficient NOD.H2 h4 mice. Additionally, we tested whether humoral or cellular immune responses of iodine-fed NOD.H2 h4 mice are preferentially directed to tg with increased iodine content (I-tg) or known pathogenic tg peptides that contained iodine. rEsULts: the iodine content of tg was not significantly different between control (9.0±2.7 I atoms per monomer) and iodine-fed mice (10.9±0.3 I atoms per monomer). Furthermore, in iodine-fed NOD.H2 h4 mice developing IsAt, strong but equivalent serum IgG responses were detected to both tg or I-tg, whereas their lymphoid cells were stimulated weakly but equally well by tg or I-tg in vitro and did not show reactivity against a panel of five pathogenic tg peptides that contained iodine. cONcLUsIONs: the results suggest that development of IsAt in NOD.H2 h4 mice is not associated with enhanced iodine organification or differential b-or t-cell responses to iodinated determinants in tg.

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“…However, this study was performed 48-72 h after addition of iodide. Under those conditions, high concentrations of iodide may induce thyroid cell injury by modulating the redox state and generating reactive oxygen species (ROS) (35)(36)(37) and inducing necrosis and apoptosis in thyroid cells (38). Cell injury results in the release of DAMPs, for Human thyroid follicles were pre-cultured for 5 days and then cultured in medium containing bovine TSH (30 lU/mL) and 10 -8 to 10 -3 M of NaI.…”

Section: Innate Immune Activation Of the Thyroid Is Induced By Iodidementioning

confidence: 99%

Demonstration of Innate Immune Responses in the Thyroid Gland: Potential to Sense Danger and a Possible Trigger for Autoimmune Reactions

Kawashima

Yamazaki²,

Hara

et al. 2013

Thyroid

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Background: Autoimmune thyroid disease is an archetypal organ-specific autoimmune disorder that is characterized by the production of thyroid autoantibodies and lymphocytic infiltration into the thyroid. However, the underlying mechanisms by which specific thyroid antibodies are produced are largely unknown. Recent studies have shown that innate immune responses affect both the phenotype and the severity of autoimmune reactions. Moreover, it appears that even non-immune cells, including thyroid cells, have an ability to launch such responses. The aim of this study was to conduct a more detailed analysis of innate immune responses of the thyroid upon stimulation with various ''non-self'' and ''self'' factors that might contribute to the initiation of autoimmune reactions. Methods: We used rat thyroid FRTL-5 cells, human thyroid cells, and mice to investigate the effects of various pathogen-associated molecular patterns (PAMPs), danger-associated molecular patterns (DAMPs), and iodide on gene expression and function that were related to innate immune responses. Results: RT-PCR analysis showed that both rat and human thyroid cells expressed mRNAs for Toll-like receptors (TLRs) that sense PAMPs. Stimulation of thyrocytes with TLR ligands resulted in activation of the interferon-beta (IFN-b) promoter and the nuclear factor kappa-light-chain-enhancer of activated B cells (NFjB)-dependent promoter. As a result, pro-inflammatory cytokines, chemokines, and type I interferons were produced. Similar activation was observed when thyroid cells were stimulated with double-stranded DNA, one of the typical DAMPs. In addition to these PAMPs and DAMPs, treatment of thyroid cells with high concentrations of iodide increased mRNA expression of various cytokines. Conclusion: We show that thyroid cells express functional sensors for exogenous and endogenous dangers, and that they are capable of launching innate immune responses without the assistance of immune cells. Such responses may relate to the development of thyroiditis, which in turn may trigger autoimmune reactions.

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Intracellular adhesion molecule-1 up-regulation on thyrocytes by iodine of non-obese diabetic.H2h4 mice is reactive oxygen species-dependent

Cited by 37 publications

References 36 publications

N-Acetylcysteine and 15 Deoxy-Δ12,14-Prostaglandin J2 Exert a Protective Effect Against Autoimmune Thyroid Destruction in Vivo but Not Against Interleukin-1α/Interferon γ-Induced Inhibitory Effects in Thyrocytes in Vitro

N-Acetylcysteine and 15 Deoxy-Δ12,14-Prostaglandin J2 Exert a Protective Effect Against Autoimmune Thyroid Destruction in Vivo but Not Against Interleukin-1α/Interferon γ-Induced Inhibitory Effects in Thyrocytes in Vitro

Iodine content of thyroglobulin in NOD.H2h4 mice developing iodine-accelerated autoimmune thyroiditis

Demonstration of Innate Immune Responses in the Thyroid Gland: Potential to Sense Danger and a Possible Trigger for Autoimmune Reactions

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