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

Shajib, Md. Sharif; Khan, Waliul I.

doi:10.1111/apha.12430

Cited by 283 publications

(248 citation statements)

References 144 publications

(305 reference statements)

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“…Human and animal studies suggest that adiposity-induced leptin increase and subsequent leptin resistance would affect these transmitters, causing or worsening asthma symptoms. This relates both to orexigenic neuropeptides such as neuropeptide Y (114)(115)(116)(117)(118)(119)(120) , endocannabinoids (121,122) , endogenous opioids (123)(124)(125)(126) ; and anorexigenic neuropeptides such as tachykinins and its most studied members substance P (127)(128)(129)(130)(131)(132) , α-melanocyte-stimulating hormone (133)(134)(135) , corticotropin-releasing factor (136)(137)(138)(139)(140)(141) and serotonin (142)(143)(144)(145)(146)(147)(148)(149)(150) . Altogether, it suggests that these peptides can modulate asthmatic inflammation among obese patients.…”

Section: Possible Linksmentioning

confidence: 99%

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

2016

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Obesity is a risk factor for asthma, and obese asthmatics have lower disease control and increased symptom severity. Several putative links have been proposed, including genetics, mechanical restriction of the chest and the intake of corticosteroids. The most consistent evidence, however, comes from studies of cytokines produced by the adipose tissue called adipokines. Adipokine imbalance is associated with both proinflammatory status and asthma. Although reverse causation has been proposed, it is now acknowledged that obesity precedes asthma symptoms. Nevertheless, prenatal origins of both conditions complicate the search for causality. There is a confirmed role of neuro-immune cross-talk mediating obesityinduced asthma, with leptin playing a key role in these processes. Obesity-induced asthma is now considered a distinct asthma phenotype. In fact, it is one of the most important determinants of asthma phenotypes. Two main subphenotypes have been distinguished. The first phenotype, which affects adult women, is characterised by later onset and is more likely to be non-atopic. The childhood obesity-induced asthma phenotype is characterised by primary and predominantly atopic asthma. In obesity-induced asthma, the immune responses are shifted towards T helper (Th) 1 polarisation rather than the typical atopic Th2 immunological profile. Moreover, obese asthmatics might respond differently to environmental triggers. The high cost of treatment of obesity-related asthma, and the burden it causes for the patients and their families call for urgent intervention. Phenotype-specific approaches seem to be crucial for the success of prevention and treatment.

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Section: Possible Linksmentioning

confidence: 99%

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

2016

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“…5-HT, in interaction with its receptor families, regulates a broad range of aspects of cognition, behavior, and physiology including mood, sleep, energy balance, tissue regeneration, platelet coagulation, and gastrointestinal functions as well as important inflammatory and immunomodulatory functions [20,48] . In particular, we associate the effect of fluoxetine treatment with the 5-HT 7 and 5-HT 2 receptors due to the associated signaling pathways, but this treatment could also modulate other immune functions mediated by the 5-HT system.…”

Section: Discussionmentioning

confidence: 99%

“…This is initially mediated by 5-HT 7 , and the phosphorylation of extracellular signal-related kinase-1 and kinase-2 (ERK1/2) and inhibitor of NFκB in T cells [20] . The activation of T cells also leads to the increased expression of 5-HT 1B and 5-HT 2A , with the former promoting T-helper (Th) cell proliferation, which leads to the differentiation and functioning of immune cells [48,49] .…”

Section: Discussionmentioning

confidence: 99%

Fluoxetine Treatment in Rats Increases the Rate of Taurine Transport in Mononuclear Cells

Colmenares-Aguilar

Urbina²,

Obregón³

et al. 2017

Neuroimmunomodulation

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Fluoxetine, a selective serotonin reuptake inhibitor antidepressant, modulates the mitogen-induced proliferation of lymphocytes. Lymphocytes contain taurine and express taurine transporter (TauT). Among the effects of taurine on lymphocytes are protection against oxidants and regulation of the inflammatory aspects of the immune response. Our aim was to determine the influence of fluoxetine treatment on taurine transport, and to determine the presence of TauT in the mononuclear cells of rats. Methods: Male adult Sprague-Dawley rats were treated with fluoxetine 10 mg/kg i.p. for 1, 2, and 3 weeks. The cells were obtained by density gradients. [³H]Taurine was used for transport assays. Amino acid levels were determined by high-performance liquid chromatography. Immunolabeling of CD4+, CD8+, and TauT was performed. The mRNA of TauT was evaluated by RT-PCR. Controls were included for each protocol. Results: The transport of taurine, after 1 week of treatment, was significantly augmented compared to controls. The affinity significantly increased at 1 and 2 weeks. While the percentage of CD4+ cells decreased and that of CD8+ cells increased, the percentage of TauT in CD4+ and CD8+ cells was not affected. Reduction of levels of aspartic acid, glutamic acid, threonine, alanine, glycine, and arginine occurred at 1 and 2 weeks. The taurine concentration significantly decreased after 2 and 3 weeks of treatment. The estimation of mRNA of TauT was not different. Conclusion: Taurine transport increases with fluoxetine treatment, and so this could be related to an immunomodulatory role of fluoxetine through TauT. Inhibition of serotonin reuptake might be involved in the regulation of taurine transport in mononuclear cells.

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“…Macrophages may be particularly relevant regarding the immunomodulatory effects of SSRIs due to their high expression of serotonin receptors [31,32] . By acting as ambient serotonin level sensors, macrophages could modulate genotype expression patterns in macrophages: activation of 5HT 7 receptors in macrophages has been noted to induce polarization towards the antiinflammatory M2 phenotype [33,34] .…”

Section: Ssri-associated Cardiometabolic Risk: Molecular Pathwaysmentioning

confidence: 99%

Metabolic risk in depression and treatment with selective serotonin reuptake inhibitors: are the metabolic syndrome and an increase in cardiovascular risk unavoidable?

Chávez-Castillo¹,

Ortega²,

Nava³

et al. 2018

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Depression is one of the most common psychiatric disorders, and has become an epidemic in modern medical practice; notorious for frequently co-occurring with multiple comorbidities, especially cardiovascular disease (CVD), type 2 diabetes mellitus (DM2), and its various risk factors comprised in the metabolic syndrome (MS). Selective serotonin reuptake inhibitors (SSRIs) are the most widely used class of psychotropic drugs in this and many other clinical scenarios; yet their impact on cardiometabolic health has not been elucidated. The objective of this review was to summarize current views on the pharmacology of SSRIs and cardiometabolic risk, as well as available epidemiological evidence regarding its clinical significance. SSRIs appear to intervene in cardiometabolic physiology fundamentally by modulating chronic inflammation, a key pathophysiologic phenomenon in MS, DM2 and CVD. However, the dosing necessary to achieve a beneficial impact in this regard, as well as their clinical correlations, remain controversial. Each SSRI displays a particular profile regarding each of the components of the MS: weight gain seems to be the most common effect of SSRIs, more frequent with paroxetine, followed by citalopram and escitalopram. As a drug class, SSRIs also appear to promote hypercholesterolemia rather uniformly, while fluoxetine and citalopram appear to particularly increase triacylglyceride levels. In contrast, fluvoxamine and paroxetine seem to have the greatest impact on dysglycemia. Lastly, most SSRIs appear to be innocuous or even beneficial regarding blood pressure and high-density lipoprotein cholesterol. Nevertheless, many of these effects may vary significantly upon specific clinical circumstances, especially timing. This topic remains rather unexplored in clinical psychopharmacology, and further, larger-scale epidemiological studies are needed in order to offer improved care in this field.

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

Cited by 283 publications

References 144 publications

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

Association between obesity and asthma – epidemiology, pathophysiology and clinical profile

Fluoxetine Treatment in Rats Increases the Rate of Taurine Transport in Mononuclear Cells

Metabolic risk in depression and treatment with selective serotonin reuptake inhibitors: are the metabolic syndrome and an increase in cardiovascular risk unavoidable?

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