Endotoxin inhibition of glucocorticoid enzyme induction and in vivo3H-dexamethasone labelling of rat liver nuclei

Vaptzarova, K. I.; Baramova, Eugenia N.; Popov, P.G.

doi:10.1016/0020-711x(89)90393-5

Cited by 4 publications

(3 citation statements)

References 23 publications

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“…In dogs treated with endotoxin, an endotoxin-induced downregulation of leukocyte GR numbers, as assayed by [ 3 H]dexamethasone binding, was also observed (Li & Xu 1988). Endotoxin inhibition of [ 3 H]dexamethasone binding was also seen in rat liver nuclei (Vaptzarova et al 1989) and peritoneal macrophages (Jiayi & Chen 1992). In bronchial epithelial cells, LPS caused an increase in GR number but also reduced the ligand affinity, as seen by an increase in the K d (Verheggen et al 1996).…”

Section: Effect Of Endotoxin On Grmentioning

confidence: 80%

Role of the hypothalamic-pituitary-adrenal axis, glucocorticoids and glucocorticoid receptors in toxic sequelae of exposure to bacterial and viral products

Webster

Sternberg

2004

Journal of Endocrinology

164

124

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The hypothalamic-pituitary-adrenal (HPA) axis is activated during many bacterial and viral infections, resulting in an increase in circulating glucocorticoid levels. This HPA axis activation and glucocorticoid response are critical for the survival of the host, as demonstrated by the fact that removal of the HPA axis (by adrenalectomy or hypophysectomy) or glucocorticoid receptor (GR) blockade enhances the severity of the infection and in some cases enhances the mortality rate. Replacement with a synthetic glucocorticoid reverses these effects by reducing the severity of the infection and provides protection against lethal effects. In addition, some bacteria and viral infections have been shown to affect the GR directly. These have been described and the implications of such an effect discussed.

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Section: Effect Of Endotoxin On Grmentioning

confidence: 80%

Role of the hypothalamic-pituitary-adrenal axis, glucocorticoids and glucocorticoid receptors in toxic sequelae of exposure to bacterial and viral products

Webster

Sternberg

2004

Journal of Endocrinology

164

124

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Section: Effect Of Bacterial Toxins On Grmentioning

confidence: 99%

“…Since the early 1980s there have been reports of decreased glucocorticoid induction of liver enzymes, including, glucose-6-phosphatase, fructose-1,6-diphosphatase, phosphenolpyruvate carboxykinase (PEPCK), tryptophan oxygenase (TO) and TAT, by endotoxin [69,70,71,72]. Several studies have shown that endotoxin decreases steroid binding sites in liver cytosol [11,70,72,73]. These effects were not only observed in liver but also in other tissues including murine macrophages [74], kidney, skeletal muscle, spleen, lung, heart tissue [70], canine leukocytes [75] and sheep lungs [76].…”

Section: Effect Of Bacterial Toxins On Grmentioning

confidence: 99%

The Glucocorticoid Receptor: A Revisited Target for Toxins

Marketon

Sternberg

2010

Toxins

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The hypothalamic-pituitary-adrenal (HPA) axis activation and glucocorticoid responses are critical for survival from a number of bacterial, viral and toxic insults, demonstrated by the fact that removal of the HPA axis or GR blockade enhances mortality rates. Replacement with synthetic glucocorticoids reverses these effects by providing protection against lethal effects. Glucocorticoid resistance/insensitivity is a common problem in the treatment of many diseases. Much research has focused on the molecular mechanism behind this resistance, but an area that has been neglected is the role of infectious agents and toxins. We have recently shown that the anthrax lethal toxin is able to repress glucocorticoid receptor function. Data suggesting that the glucocorticoid receptor may be a target for a variety of toxins is reviewed here. These studies have important implications for glucocorticoid therapy.

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Are serotonergic mechanisms involved in the acute toxicity of chlorinated dibenzo-p-dioxins (CDDs)?

1992

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Endotoxin inhibition of glucocorticoid enzyme induction and in vivo3H-dexamethasone labelling of rat liver nuclei

Cited by 4 publications

References 23 publications

Role of the hypothalamic-pituitary-adrenal axis, glucocorticoids and glucocorticoid receptors in toxic sequelae of exposure to bacterial and viral products

Role of the hypothalamic-pituitary-adrenal axis, glucocorticoids and glucocorticoid receptors in toxic sequelae of exposure to bacterial and viral products

The Glucocorticoid Receptor: A Revisited Target for Toxins

Are serotonergic mechanisms involved in the acute toxicity of chlorinated dibenzo-p-dioxins (CDDs)?

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