Zymosan-induced luminol-amplified chemiluminescence of whole blood phagocytes in experimental and human hyperthyroidism

Videla, Luis A.; Correa, Loreto; Rivera, Marcela; Sir, Teresa

doi:10.1016/0891-5849(93)90149-o

Cited by 33 publications

(23 citation statements)

References 17 publications

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“…Some authors find that in vitro TH stimulation increases neutrophil ROS generation (Mezosi et al 2005), whereas others only find an effect for supraphysiological levels of T 4 (Marino et al 2006). In contrast, a decrease in ROS generation after TH incubation (Aoyagi et al 1991) or no effect at all has also been reported (Videla et al 1993). These conflicting results suggest that the effects of TH on neutrophil ROS generation cannot be entirely explained by direct effects of TH on these cells.…”

Section: Effects Of Thyroid Hormones On Neutrophil Functionmentioning

confidence: 38%

“…Several studies in both human subjects and animal models have found that, similar to neutrophils, stimulated hyperthyroid macrophages have increased ROS production ex vivo (Videla et al 1993, Magsino et al 2000 although one study found an opposite effect (Rosa et al 1995). PTU treatment of hyperthyroid patients normalized ROS production although these findings could not be replicated in vitro (Videla et al 1993).…”

Section: Effects Of Extracellular Thyroid Hormone Levels On Macrophagmentioning

confidence: 68%

“…In general, incubation with TH appears to have a pro-inflammatory effect in these cells. This is illustrated by the fact that ROS production and MPO activity are increased in hyperthyroid neutrophils (Videla et al 1993, Fernandez & Videla 1995, Szabo et al 1996, Magsino et al 2000, Mezosi et al 2005, Russo-Carbolante et al 2005b, Marino et al 2006. Higher TH levels also increase reactive nitrogen species production, phagocytosis and bacterial killing in macrophages , Chen et al 2012.…”

Section: Discussionmentioning

confidence: 96%

“…PTU treatment of hyperthyroid patients normalized ROS production although these findings could not be replicated in vitro (Videla et al 1993). It should be noted that the majority of these studies assessed a mixed population of mononuclear cells containing significant numbers of other cell types, making it impossible to determine the contribution of the macrophage/monocyte subset.…”

Section: Effects Of Extracellular Thyroid Hormone Levels On Macrophagmentioning

confidence: 87%

“…Hyperthyroidism results in increased ROS generation by stimulated neutrophils ex vivo compared to cells from euthyroid controls, whereas hypothyroidism has the opposite effect and limits neutrophil ROS generation. This has been demonstrated in neutrophils from hypothyroid and hyperthyroid rats (Videla et al 1993, Fernandez & Videla 1995 and hyperthyroid and hypothyroid patients (Videla et al 1993, Szabo et al 1996, Russo-Carbolante et al 2005b, Marino et al 2006 or healthy controls with experimentally induced hyperthyroidism (Magsino et al 2000). In both hypothyroidism and 232:2 hyperthyroidism, the changes in neutrophil ROS generation are (partially) reversed by restoring TH levels to within the normal range (Videla et al 1993, Marino et al 2006.…”

Section: Effects Of Thyroid Hormones On Neutrophil Functionmentioning

confidence: 89%

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Thyroid hormone metabolism in innate immune cells

Spek

Fliers

Boelen

2017

Journal of Endocrinology

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Thyroid hormone (TH) metabolism and thyroid status have been linked to various aspects of the immune response. There is extensive literature available on the effects of thyroid hormone on innate immune cells. However, only recently have authors begun to study the mechanisms behind these effects and the role of intracellular TH metabolism in innate immune cell function during inflammation. This review provides an overview of the molecular machinery of intracellular TH metabolism present in neutrophils, macrophages and dendritic cells and the role and effects of intracellular TH metabolism in these cells. Circulating TH levels have a profound effect on neutrophil, macrophage and dendritic cell function. In general, increased TH levels result in an amplification of the pro-inflammatory response of these cells. The mechanisms behind these effects include both genomic and non-genomic effects of TH. Besides a pro-inflammatory effect induced by extracellular TH, the cellular response to pro-inflammatory stimuli appears to be dependent on functional intracellular TH metabolism. This is illustrated by the fact that the deiodinase enzymes and in some cell types also thyroid hormone receptors appear to be crucial for adequate innate immune cell function. This overview of the literature suggests that TH metabolism plays an important role in the host defence against infection through the modulation of innate immune cell function.

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Section: Effects Of Thyroid Hormones On Neutrophil Functionmentioning

confidence: 38%

Section: Effects Of Extracellular Thyroid Hormone Levels On Macrophagmentioning

confidence: 68%

Section: Discussionmentioning

confidence: 96%

Section: Effects Of Extracellular Thyroid Hormone Levels On Macrophagmentioning

confidence: 87%

Section: Effects Of Thyroid Hormones On Neutrophil Functionmentioning

confidence: 89%

See 3 more Smart Citations

Thyroid hormone metabolism in innate immune cells

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Fliers

Boelen

2017

Journal of Endocrinology

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Effect of thyroid hormone administration on the depletion of circulating glutathione in the isolated perfused rat liver and its relationship to basolateral γ‐glutamyltransferase activity

Videla

Fernández

1995

J. Biochem. Toxicol.

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The influence of thyroid hormone administration on liver glutathione (GSH) extraction in the isolated perfused liver was studied in fed rats for a period of 1-7 days following a single dose of 0.1 mg 3,5,3'-triiodothyronine (T3)/kg. T3 treatment led to an early and transient calorigenic response, as well as an enhancement in liver GSH removal, reaching a maximal effect at 2 days after hormone administration, which was normalized in the 3- to 7-day period studied. Addition of the gamma-glutamyltransferase (gamma-GT) inhibitor DL-serineborate (4 mM) to the perfusate abolished the increase in the hepatic removal of GSH elicited by T3, and enhanced the sinusoidal concentration of GSH, studied at 2 days after hormone administration. These data support the role of hepatic basolateral gamma-GT ectoactivity in the depletion of portally added and liver-derived GSH as an adaptive response to recover GSH levels after reduction by T3-induced oxidative stress.

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Thyroid Gland in Free Radical-Induced Oxidative Stress

Kale

2014

Free Radicals in Human Health and Disease

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Zymosan-induced luminol-amplified chemiluminescence of whole blood phagocytes in experimental and human hyperthyroidism

Cited by 33 publications

References 17 publications

Thyroid hormone metabolism in innate immune cells

Thyroid hormone metabolism in innate immune cells

Effect of thyroid hormone administration on the depletion of circulating glutathione in the isolated perfused rat liver and its relationship to basolateral γ‐glutamyltransferase activity

Thyroid Gland in Free Radical-Induced Oxidative Stress

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