Serotonin as a Modulator of Immune Function: An Overview

Cloëz‐Tayarani, Isabelle

doi:10.2174/157339506775471893

Cited by 12 publications

(2 citation statements)

References 81 publications

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“…Moreover, even considering the inhibitory effect of a 5‐HT 1A receptor antagonist (WAY100638), it cannot be excluded that 5‐HT might have activated other 5‐HT receptor subtypes. Indeed, both 5‐HT 3A and 5‐HT 4 have been found on monocytes and might be sensitive to relatively high doses of 5‐HT 1A receptor antagonist, such as the one used in our study ( Cloez‐Tayarani, 2006 ; Cloez‐Tayarani and Changeux, 2007 ). Moreover, although 8‐OH DPAT is considered a selective agonist for the 5‐HT 1A receptor, it can also act as a partial agonist at 5‐HT 7 receptors ( Bard et al ., 1993 ; Shen et al ., 1993 ).…”

Section: Discussionmentioning

confidence: 90%

Serotonin decreases HIV‐1 replication in primary cultures of human macrophages through 5‐HT_1A receptors

Manéglier

Guillemin

Clayette

et al. 2008

British J Pharmacology

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Background and purpose: 5-HT (serotonin) is known to be involved in neuroinflammation and immunoregulation. The human immunodeficiency virus (HIV) targets cells such as monocytes/macrophages, which colocalize with 5-HT-releasing cell types, mostly platelets. In this study, we investigated the effects of 5-HT on HIV-1-infected macrophages in vitro. Experimental approach: Human macrophages cultured in serum-free medium were treated over 7 days with 5-HT at three concentrations (0.01, 1 and 100 mM) with or without agonists and antagonists of 5-HT 1A and 5-HT 2 receptors. After 7 days of treatment, macrophages were infected with HIV-1/Ba-L and virus replication was monitored over 16 days and expression of proviral HIV DNA was investigated by PCR after 24 h of infection. Cell surface expression of HIV-1/Ba-L receptor (CD4) and coreceptor (CCR5) was investigated by flow cytometry. The CCR5 ligand, macrophage inflammatory protein-1a (MIP-1a), was quantified by ELISA in cell culture supernatants and MIP-1a mRNA expression was assessed by reverse transcriptase-PCR. Key results: In vitro, 5-HT downregulated the membranous expression of CCR5 and led to a decrease of HIV-1 infection, probably through its action on 5-HT 1A receptors. 5-HT (100 mM) was also able to induce overexpression of MIP-1a mRNA leading to an increase of MIP-1a secretion by human macrophages. Conclusions and implications:The effects of 5-HT on HIV infection could be a consequence of the increase in MIP-1a concentrations and/or CCR5 receptor downregulation. These results suggest that 5-HT can inhibit the replication of HIV-1 in primary culture of human macrophages through its action on 5-HT 1A receptors.

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Section: Discussionmentioning

confidence: 90%

Serotonin decreases HIV‐1 replication in primary cultures of human macrophages through 5‐HT_1A receptors

Manéglier

Guillemin

Clayette

et al. 2008

British J Pharmacology

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“…5‐HT levels are also elevated in affected synovial fluid, released by activated platelets, and induces synovial plasma extravasation by the release of various inflammatory mediators (Wang et al . , Cloëz‐Tayarani , Seidel et al . ).…”

Section: ‐Ht In Inflammationmentioning

confidence: 99%

The role of serotonin and its receptors in activation of immune responses and inflammation

2014

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Serotonin or 5-hydroxytryptamine (5-HT) is a neurotransmitter and hormone that contributes to the regulation of various physiological functions by its actions in the central nervous system (CNS) and in the respective organ systems. Peripheral 5-HT is predominantly produced by enterochromaffin (EC) cells of the gastrointestinal (GI) tract. These gut-resident cells produce much more 5-HT than all neuronal and other sources combined, establishing EC cells as the main source of this biogenic amine in the human body. Peripheral 5-HT is also a potent immune modulator and affects various immune cells through its receptors and via the recently identified process of serotonylation. Alterations in 5-HT signalling have been described in inflammatory conditions of the gut, such as inflammatory bowel disease. The association between 5-HT and inflammation, however, is not limited to the gut, as changes in 5-HT levels have also been reported in patients with allergic airway inflammation and rheumatoid arthritis. Based on searches for terms such as '5-HT', 'EC cell', 'immune cells' and 'inflammation' in pubmed.gov as well as by utilizing pertinent reviews, the current review aims to provide an update on the role of 5-HT in biological functions with a particular focus on immune activation and inflammation.

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Serotonin mediates PGE2 overexpression through 5-HT2A and 5-HT3 receptor subtypes in serum-free tissue culture of macrophage-like synovial cells

et al. 2008

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Serotonin antagonists show impressive analgesic efficacy in rheumatoid arthritis, osteoarthritis (OA) or fibromyalgia; however, this effect is not well understood. We examined the mechanism of serotonin-induced inflammation and its antagonists in OA. Serotonin receptor subtypes and COX-2 were analysed by RT-PCR from synovial tissue. Serum-free cultures were stimulated with 10 muM serotonin and/or the antagonists ketanserin (5-HT(2A)), tropisetron (5-HT(3)) and parecoxib (COX-2). Prostaglandin E(2) (PGE(2)), tumour necrosis factor alpha (TNF-alpha), interleukin 1beta (IL-1beta) and leukotriene B4 (LTB4) were measured by an immunoassay in the supernatants. RT-PCR results showed mRNA for 5-HT(2A) and 5-HT(3) receptors, and COX-2. PGE(2) in the supernatants increased by 261.2% +/- 56.7 (mean +/- SEM; P = 0.007) in response to serotonin. TNF-alpha, IL-1beta and LTB4 levels did not change. Ketanserin, tropisetron and parecoxib suppressed PGE(2). The serotonin-induced PGE(2) overexpression appeared thus to be mediated by 5-HT(2A) and 5-HT(3) receptors. This activation might involve COX-2. The findings may explain the potent benefit of 5-HT(3) antagonists.

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Serotonin as a Modulator of Immune Function: An Overview

Cited by 12 publications

References 81 publications

Serotonin decreases HIV‐1 replication in primary cultures of human macrophages through 5‐HT_1A receptors

Serotonin decreases HIV‐1 replication in primary cultures of human macrophages through 5‐HT_1A receptors

The role of serotonin and its receptors in activation of immune responses and inflammation

Serotonin mediates PGE2 overexpression through 5-HT2A and 5-HT3 receptor subtypes in serum-free tissue culture of macrophage-like synovial cells

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Serotonin as a Modulator of Immune Function: An Overview

Cited by 12 publications

References 81 publications

Serotonin decreases HIV‐1 replication in primary cultures of human macrophages through 5‐HT1A receptors

Serotonin decreases HIV‐1 replication in primary cultures of human macrophages through 5‐HT1A receptors

The role of serotonin and its receptors in activation of immune responses and inflammation

Serotonin mediates PGE2 overexpression through 5-HT2A and 5-HT3 receptor subtypes in serum-free tissue culture of macrophage-like synovial cells

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Product

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Serotonin decreases HIV‐1 replication in primary cultures of human macrophages through 5‐HT_1A receptors

Serotonin decreases HIV‐1 replication in primary cultures of human macrophages through 5‐HT_1A receptors