Alterations in thyroid hormone economy during acute infection with Diplococcus pneumoniae in the rhesus monkey

Woeber, Kenneth A.; Harrison, William A.

doi:10.1172/jci106505

Cited by 39 publications

(42 citation statements)

References 14 publications

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“…Activated phagocytosing neutrophils are capable of cleavage of thyroxinebinding globulin (TBG), thus increasing the amount of extracellularly available T 4 (Jirasakuldech et al 2000). As mentioned previously, phagocytosing neutrophils also metabolize significant amounts of TH (Woeber 1971, Woeber et al 1972, Klebanoff & Green 1973, Woeber & Ingbar 1973. This suggests that TH metabolism plays an important role in infiltrating neutrophils during infection.…”

Section: Role Of Intracellular Thyroid Hormone Metabolism In Neutrophmentioning

confidence: 80%

“…Murine neutrophils contain the TH transporter MCT8, whereas human neutrophils express MCT10 but not MCT8 mRNA (Boelen et al 2005, van der Spek et al 2016. It has long been known that activated neutrophils are capable of deiodinating both T 3 and T 4 (Woeber 1971, Woeber et al 1972, Klebanoff & Green 1973, Woeber & Ingbar 1973. Research from the seventies already found that phagocytosing human neutrophils can generate both T 3 and rT 3 from T 4 and that this deiodinating activity was mainly present in the granule fraction of the cells (Woeber 1976(Woeber , 1978.…”

Section: Intracellular Thyroid Hormone Metabolism In Neutrophilsmentioning

confidence: 99%

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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: Role Of Intracellular Thyroid Hormone Metabolism In Neutrophmentioning

confidence: 80%

Section: Intracellular Thyroid Hormone Metabolism In Neutrophilsmentioning

confidence: 99%

Thyroid hormone metabolism in innate immune cells

Spek

Fliers

Boelen

2017

Journal of Endocrinology

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“…Healthy, male rhesus monkeys (Macaca nitlatta) weighing between 2.5 and 4.3 kg were placed in primate chairs, fed a standard or iodine-deficient diet (2), and allowed water ad lib. Rectal temperatures, complete blood counts, and blood cultures were obtained frequently, as indicated in the results.…”

Section: Methodsmentioning

confidence: 99%

“…Accelerated metabolism of the thyroid hormones has been observed during acute pneumococcal infections in man and the rhesus monkey (1,2). In the monkey, cellular uptake of L-thyroxine (T4) 'is enhanced during the early course of this illness (3).…”

Section: Introductionmentioning

confidence: 99%

“…The pathogenesis and significance of these alterations in the distribution and metabolism of the thyroid hormones during infection are not clear. Studies with peripheral leukocytes in vitro suggest that these alterations might constitute a host defense mechanism in which phagocytozing cells utilize thyroid hormone as a source of iodine in a peroxidase-hydrogen peroxidehalide system for the iodination and killing of ingested microorganisms (2,(5)(6)(7)(8)(9). However, the extent to which iodide or the thyroid hormones participate in vivo in this putative antimicrobial system remains uncertain (6,10,11).…”

Section: Introductionmentioning

confidence: 99%

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Accelerated Cellular Uptake and Metabolism of L-Thyroxine during Acute Salmonella typhimurium Sepsis

DeRubertis¹,

Woeber²

1973

J. Clin. Invest.

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A B S T R A C T The effects of acute Salmonella typhimurium sepsis on the kinetics of peripheral L-thyroxine (T4) distribution and metabolism and on serum total and free T4 concentrations were studied in rhesus monkeys inoculated i.v. with either heat-killed or viable organisms. The rate of disappearance of labeled T4 from serum was increased within 8 h after inoculation of monkeys with either heat-killed or viable Salmonella. The effects of the heat-killed organisms were transient and no longer evident by 16 h postinoculation. The monkeys inoculated with the viable Salmonella experienced a 2-3 day febrile, septic illness that was accompanied by an increase in the absolute rate of T4 disposal. In the infected monkeys, serum total T4 and endogenously labeled protein-bound iodine concentrations fell significantly during the period of acute sepsis and then rose during convalescence to values that exceeded the preinoculation values, suggesting that thyroidal secretion of hormone had increased in response to a primary depletion of the peripheral hormonal pool. Total cellular and hepatic uptakes of T4 were enhanced by 4 h after inoculation of monkeys with either heatkilled or viable Salmonella, but the increase in total cellular uptake persisted for 24 h only in the monkeys inoculated with the viable organisms. These alterations in T4 kinetics could neither be correlated with changes in the binding of T4 in plasma nor attributed to an increase in vascular permeability. Moreover, they could not be ascribed to an in vitro product of bacterial growth, suggesting that the presence of the organisms themselves was required. An acceleration of T4 disappearance was also observed during Escherichia coli and Diplococcus pneumioniae bacteremias. Our findings are Dr. Woeber's present address is the

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The Thyroid Gland

Bürgi¹

1986

Clinical Endocrinology

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Alterations in thyroid hormone economy during acute infection with Diplococcus pneumoniae in the rhesus monkey

Cited by 39 publications

References 14 publications

Thyroid hormone metabolism in innate immune cells

Thyroid hormone metabolism in innate immune cells

Accelerated Cellular Uptake and Metabolism of L-Thyroxine during Acute Salmonella typhimurium Sepsis

The Thyroid Gland

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