Microarray analysis of transcription factor gene expression in melatonin‐treated human peripheral blood mononuclear cells

Ha, Eunyoung; Han, Earl; Kim, Hak-Jae; Hong, Mee Suk; Hong, Seung‐Jae; Yoon, Kyung Sik; Kang, Insug; Cho, Yong Hoo; Chung, Joo‐Ho; Yim, Sung-Vin; Baik, Hee Jung

doi:10.1111/j.1600-079x.2006.00317.x

Cited by 19 publications

(22 citation statements)

References 35 publications

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“…Concretely, the ASMT gene is strongly expressed in the Th cells (CD14 − CD4 + ) and cytotoxic T cells (CD56 − CD8 + ) . Moreover, the activation of AA‐NAT and ASMT leads to the release of abundant amounts of melatonin and the inhibition of ASMT or TPH correspondingly reduces melatonin release . Thus, the physiological state of melatonin synthase may play an important role in T‐cell activation, which is consistent with the finding that T‐cell activation is associated with the endogenous synthesis of melatonin in T cells …”

Section: Activation and Proliferation Of Intestinal Mucosal Immune Cesupporting

confidence: 83%

Melatonin mediates mucosal immune cells, microbial metabolism, and rhythm crosstalk: A therapeutic target to reduce intestinal inflammation

Zhang

Reíter

et al. 2019

Medicinal Research Reviews

121

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Nowadays, melatonin, previously considered only as a pharmaceutical product for rhythm regulation and sleep aiding, has shown its potential as a co‐adjuvant treatment in intestinal diseases, however, its mechanism is still not very clear. A firm connection between melatonin at a physiologically relevant concentration and the gut microbiota and inflammation has recently established. Herein, we summarize their crosstalk and focus on four novelties. First, how melatonin is synthesized and degraded in the gut and exerts potentially diverse phenotypic effects through its diverse metabolites. Second, how melatonin mediates the activation and proliferation of intestinal mucosal immune cells with paracrine and autocrine properties. By modulating T/B cells, mast cells, macrophages and dendritic cells, melatonin immunomodulatory involved in regulating T‐cell differentiation, intervening T/B cell interaction and attenuating the production of pro‐inflammatory factors, achieving its antioxidant action via specific receptors. Third, how melatonin exerts antimicrobial action and modulates microbial components, such as lipopolysaccharide, amyloid‐β peptides via nuclear factor κ‐light‐chain‐enhancer of activated B cells (NF‐κB) or signal transducers and activators of transcription (STAT1) pathway to modulate intestinal immune function in immune‐pineal axis. The last, how melatonin mediates the effect of intestinal bacterial activity signals on the body rhythm system through the NF‐κB pathway and influences the mucosal epithelium oscillation via clock gene expression. These processes are achieved at mitochondrial and nuclear levels to control the host immune cell development. Considering unclear mechanisms and undiscovered actions of melatonin in gut‐microbiome‐immune axis, it's time to reveal them and provide new insight for the outlook of melatonin as a potential therapeutic target in the treatment and management of intestinal diseases.

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Section: Activation and Proliferation Of Intestinal Mucosal Immune Cesupporting

confidence: 83%

Melatonin mediates mucosal immune cells, microbial metabolism, and rhythm crosstalk: A therapeutic target to reduce intestinal inflammation

Zhang

Reíter

et al. 2019

Medicinal Research Reviews

121

View full text Add to dashboard Cite

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“…In addition to TPH and AADC, T cells also express NAT and HIOMT. Resting PBMCs and PBMCs activated by PHA express NAT and HIOMT and release abundant amounts of melatonin into the culture media . Inhibition of either HIOMT or TPH reduces the release of melatonin from resting PBMCs or PHA‐activated PBMCs .…”

Section: Melatonin Signaling In T Cellsmentioning

confidence: 99%

“…Resting PBMCs and PBMCs activated by PHA express NAT and HIOMT and release abundant amounts of melatonin into the culture media. 38,93 Inhibition of either HIOMT or TPH reduces the release of melatonin from resting PBMCs or PHA-activated PBMCs. 38 Furthermore, T helper cells (CD14 − CD4 + ) and cytotoxic T cells (CD56 − CD8 + ) from human PBMCs strongly express the HIOMT gene.…”

Section: Melatonin Signaling In T Cellsmentioning

confidence: 99%

Melatonin signaling in T cells: Functions and applications

Ren

Liu

Chen

et al. 2017

Journal of Pineal Research

187

130

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Melatonin affects a variety of physiological processes including circadian rhythms, cellular redox status, and immune function. Importantly, melatonin significantly influences T-cell-mediated immune responses, which are crucial to protect mammals against cancers and infections, but are associated with pathogenesis of many autoimmune diseases. This review focuses on our current understanding of the significance of melatonin in T-cell biology and the beneficial effects of melatonin in T-cell response-based diseases. In addition to expressing both membrane and nuclear receptors for melatonin, T cells have the four enzymes required for the synthesis of melatonin and produce high levels of melatonin. Meanwhile, melatonin is highly effective in modulating T-cell activation and differentiation, especially for Th17 and Treg cells, and also memory T cells. Mechanistically, the influence of melatonin in T-cell biology is associated with membrane and nuclear receptors as well as receptorindependent pathways, for example, via calcineurin. Several cell signaling pathways, including ERK1/2-C/EBPα, are involved in the regulatory roles of melatonin in Tcell biology. Through modulation in T-cell responses, melatonin exerts beneficial effects in various inflammatory diseases, such as type 1 diabetes, systemic lupus erythematosus, and multiple sclerosis. These findings highlight the importance of melatonin signaling in T-cell fate determination, and T cell-based immune pathologies. K E Y W O R D Smelatonin, multiple sclerosis, systemic lupus erythematosus, T cells, Th17 cells, Treg cells

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“…Melatonin is a sleep promoter and a chemical signal of light and darkness. Moreover, this hormone is a free radical scavenger and broad-spectrum antioxidant and has well-documented immunomodulatory effects (8) in part by modifying gene expression in inflammatory cells (22). There are some studies reporting the protective effects of this hormone in sepsis in both humans and animals, decreasing the levels of inflammatory cytokines and oxidative stress (20,21).…”

mentioning

confidence: 99%

Effects of melatonin in an experimental model of ventilator-induced lung injury

Pedreira

García-Prieto

Parra

et al. 2008

American Journal of Physiology-Lung Cellular and Molecular Phys

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Melatonin is a free radical scavenger and a broad-spectrum antioxidant and has well-documented immunomodulatory effects. We studied the effects of this hormone on lung damage, oxidative stress, and inflammation in a model of ventilator-induced lung injury (VILI), using 8- to 12-wk-old Swiss mice ( n = 48). Animals were randomized into three experimental groups: control (not ventilated); low-pressure ventilation [peak inspiratory pressure 15 cmH2O, positive end-expiratory pressure (PEEP) 2 cmH2O], and high-pressure ventilation (peak inspiratory pressure 25 cmH2O, PEEP 0 cmH2O). Each group was divided into two subgroups: eight animals were treated with melatonin (10 mg/kg ip, 30 min before the onset of ventilation) and the remaining eight with vehicle. After 2 h of ventilation, lung injury was evaluated by gas exchange, wet-to-dry weight ratio, and histological analysis. Levels of malondialdehyde, glutathione peroxidase, interleukins IL-1β, IL-6, TNF-α, and IL-10, and matrix metalloproteinases 2 and 9 in lung tissue were measured as indicators of oxidation status, pro-/anti-inflammatory cytokines, and matrix turnover, respectively. Ventilation with high pressures induced severe lung damage and release of TNF-α, IL-6, and matrix metalloproteinase-9. Treatment with melatonin improved oxygenation and decreased histological lung injury but significantly increased oxidative stress quantified by malondialdehyde levels. There were no differences in TNF-α, IL-1β, IL-6, or matrix metalloproteinases caused by melatonin treatment, but IL-10 levels were significantly higher in treated animals. These results suggest that melatonin decreases VILI by increasing the anti-inflammatory response despite an unexpected increase in oxidative stress.

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Microarray analysis of transcription factor gene expression in melatonin‐treated human peripheral blood mononuclear cells

Cited by 19 publications

References 35 publications

Melatonin mediates mucosal immune cells, microbial metabolism, and rhythm crosstalk: A therapeutic target to reduce intestinal inflammation

Melatonin mediates mucosal immune cells, microbial metabolism, and rhythm crosstalk: A therapeutic target to reduce intestinal inflammation

Melatonin signaling in T cells: Functions and applications

Effects of melatonin in an experimental model of ventilator-induced lung injury

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