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ABSTRACT
In the present study the effects of insulin, glucocorticoids and thyroid hormones on macrophage metabolism and function were investigated. The maximum activities of hexokinase, glucose-6-phosphate dehydrogenase, glutaminase and citrate synthase were determined in macrophages obtained from hormonetreated rats and those cultured for a period of 48 h in the presence of hormones. Macrophage phagocytosis was markedly inhibited by dexamethasone and thyroid hormones, remaining unchanged when insulin was added to the culture medium, however. The changes in the enzyme activities caused by hormone treatments of the rats were very similar to those found in culture. Insulin enhanced citrate synthase and hexokinase activities and diminished those of glutaminase and glucose-6-phosphate dehydrogenase. Dexamethasone had a similar effect except on glucose6-phosphate dehydrogenase. The addition of thyroid hormones to the culture medium raised the activities of glutaminase and hexokinase and reduced that of citrate synthase. The results presented support the suggestion that the effects of insulin, glucocorticoids and thyroid hormones on immune and inflammatory responses could well be mediated through changes in macrophage metabolism..
Journal of Endocrinology (1992) 135, 213–219
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recognized as a proinflammatory and pro-atherogenic cytokine ( Cho et al. 2009 , Wolak 2014 ). In the progress of atherosclerosis, OPN have been shown to be highly expressed in macrophages, vascular smooth muscle cells (VSMCs) and endothelial cells (ECs
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Abstract
In this study, we provide the first report on the production of granulocyte-macrophage colony-stimulating factor (GM-CSF) by human thyroid epithelial cells. Primary cultures of highly purified thyrocytes and thyroid-derived fibroblasts (n=3) and three thyroid anaplastic and one largely papillary carcinoma cell lines were exposed to different potent GM-CSF stimulators, employing interleukin 1α (Il-1α) and tumour necrosis factor-α (TNF-α). Cytokine mRNA levels were monitored by semiquantitative reverse transcriptase-PCR including an internal heterologous competitor fragment after 3, 6 and 18 h of culture. Culture supernatants were assayed for GM-CSF using a highly sensitive ELISA (detection limit ≤ 0·5 pg/ml) after 24 h.
Basal GM-CSF mRNA expression was higher in fibroblasts and SW 1736 cells compared with thyrocytes, C 634, 8505 C and HTh 74 cells. GM-CSF was spontaneously secreted by fibroblasts (means ± s.e.m.; 43 ± 15 pg/ml), SW 1736 (59 ± 4 pg/ml), HTh 74 (34 ± 4 pg/ml) and C 643 cells (12 ± 1 pg/ml) but not by thyrocytes and 8505 C cells. Treatment with Il-1α (10 U/ml) resulted in a marked increase of GM-CSF mRNA within 3 h and an increase or induction of protein expression in thyrocyte (2350 ± 214 pg/ml), fibroblast (5242 ± 1400 pg/ml), SW 1736 (20016 ± 280 pg/ml) and C 643 cultures (1285 ± 79 pg/ml). Stimulation with TNF-α (10 U/ml) yielded divergent results. No significant increase of GM-CSF mRNA or protein expression was found in thyrocytes although TNF-α receptor expression in these cells is well documented. Stimulation with TNF-α resulted in an increased GM-CSF production in fibroblasts (361 ± 14 pg/ml), HTh 74 (148 ± 51 pg/ml) and SW 1736 cultures (235 ± 43 pg/ml). TSH (10 mU/ml) did not stimulate GM-CSF secretion in thyrocytes and HTh 74 cells, both expressing the TSH receptor. Phorbol 12-myristate 13-acetate (10 ng/ml) enhanced GM-CSF mRNA and protein levels in all cell types investigated.
Our data suggest that both thyrocytes and fibroblasts synthesize GM-CSF in response to Il-1α, but only fibroblasts respond to TNF-α with a significant increase in GM-CSF. Anaplastic thyroid carcinomas are potential GM-CSF producers.
Journal of Endocrinology (1996) 151, 277–285
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Abstract
Stimulation of human peripheral blood monocytes with the thyroid hormones tri-iodothyronine (T3) and thyroxine (T4) enhanced their ability to mature into cytologically and functionally characteristic veiled/dendritic cells. Veiled/dendritic cell transition induced by T3 and T4 was dependent on the production of granulocyte-macrophage colony-stimulating factor (GM-CSF), tumour necrosis factor-α (TNFα) and interleukin-6 (IL-6) in the culture, since the addition of antibodies specific for GM-CSF, TNFα and IL-6 to the culture system had blocking effects. The addition of antibodies to macrophage colony-stimulating factor and IL-1 had no effects. Contaminating T cells and B cells did not contribute to the transition of monocytes to veiled/dendritic cells, and it is therefore likely that the GM-CSF, TNFα and IL-6 produced in the culture system were derived from the monocytes themselves.
Stimulation of the blood monocytes with an optimal concentration of metrizamide (14·5%), reverse T3 (rT3; 2 × 10−10 m) or highly iodinated thyroglobulin (Tg; 2 × 10−11 m) also resulted in an increased transition of monocytes to veiled/dendritic cells, but to a lesser extent in comparison with the thyroid hormones (T3, 31 ±6% and T4, 25 ±5% vs rT3, 22 ± 8% and Tg with an iodination grade of 0·37%: 20 ± 4% veiled/dendritic cells). Administration of anti-GM-CSF, anti-TNFα and anti-IL-6 to the culture system also had blocking effects on the transition from monocytes to veiled/dendritic cells induced by the iodinated compounds. The mechanisms by which such iodinated compounds act on the monocyte to veiled/dendritic cell transition can only be speculated on (interference H2O2-generating system?).
Journal of Endocrinology (1994) 140, 503–512
Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia
Department of Endocrinology and Diabetes, Fiona Stanley Hospital, Murdoch, Western Australia, Australia
Department of General Medicine, Sir Charles Gairdner Hospital, Nedlands, Western Australia, Australia
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Department of Nephrology, Monash Medical Centre, Clayton, Victoria, Australia
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Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia
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Royal College of Surgeons in Ireland, Dublin, Ireland
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Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia
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Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia
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Department of Molecular and Translational Sciences, Monash University, Clayton, Victoria, Australia
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inhibition of epithelial MR and associated adverse effects ( Tesch & Young 2017 ). Specifically, we identified monocyte-macrophages as a key cell type in which MR regulates pro-inflammatory cytokine release, ECM degradation and exacerbation of cardiac
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Pediatrics, Division of Neurosciences, Pape Pediatric Research Institute
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act in an adipocyte-autonomous way, whereas others are mediated by macrophage polarization. Macrophages can obtain distinct functional phenotypes, M1 and M2, via different polarization responses to environmental stimuli. M1 phenotypes are stimulated
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Department of Endocrinology, Renmin Hospital of Wuhan University, Wuhan, Hubei, China
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Drug Discovery Center, Key Laboratory of Chemical Genomics, Peking University Shenzhen Graduate School, Shenzhen, China
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effective approaches for treatment and/or prevention of obesity-associated metabolic diseases. Since the discovery of macrophage infiltration in adipose tissue of mice with diet-induced obesity (DIO) ( Weisberg et al. 2003 , Xu et al. 2003 ), a
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Department of Endocrinology, Renmin Hospital, Wuhan University, Wuhan, Hubei, China
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Department of Endocrinology, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
The Laboratory of Lipid & Glucose Metabolism, The First Affiliated Hospital of Chongqing Medical University, Chongqing, China
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Department of Geriatrics, Nanjing Drum Tower Hospital, the Affiliated Nanjing Hospital of Nanjing University Medical School, Nanjing, Jiangshu, China
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Department of Endocrinology, The Third Affiliated Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China
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Beijing Advanced Innovation Center for Food Nutrition and Human Health, College of Food Science & Nutritional Engineering, China Agricultural University, Beijing, China
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such as macrophages and neutrophils ( Gessi et al. 2000 , Haskó et al. 2008 ). Previous studies have validated a critical role for A 2A R in the pathophysiology of NAFLD/NASH. Specifically, A 2A R activation is shown to ameliorate NASH phenotype in
