5-Hydroxytryptamine Induces Mast Cell Adhesion and Migration

Kushnir-Sukhov, Nataliya M.; Gilfillan, Alasdair M.; Coleman, John W.; Brown, Jared M.; Bruening, S.; Tóth, Miklós; Metcalfe, Dean D.

doi:10.4049/jimmunol.177.9.6422

Cited by 131 publications

(116 citation statements)

References 52 publications

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“…Serotonin receptors belong to the G-protein-coupled receptor family with exception of the 5-HT 3 receptor, which is an ion channel (Barnes and Sharp, 1999). Despite the major role of 5-HT in the CNS, ∼90% of 5-HT is produced in the gastro-intestinal tract (Racké et al, 1996), where it is involved in the regulation of multiple physiological processes such as stimulation of cytokine and chemokine production (Dürk et al, 2005;Idzko et al, 2004;Müller et al, 2009), cell proliferation (Pakala and Benedict, 1998;Pakala et al, 1997), migration (Kushnir-Sukhov et al, 2006;Müller et al, 2009;Tamura et al, 1997) and the regulation of the immune system (Ahern, 2011). Expression of 5-HT receptors has been identified on a broad range of immune cells, including T cells (O'Connell et al, 2006), macrophages (Mikulski et al, 2010) and dendritic cells (Idzko et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

Serotonin receptor 5-HT7 regulates morphology and migratory properties of dendritic cells

Holst

Guseva

Schindler

et al. 2015

Journal of Cell Science

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Dendritic cells are potent antigen-presenting cells endowed with the unique ability to initiate adaptive immune responses upon inflammation. Inflammatory processes are often associated with an increased production of serotonin, which operates by activating specific receptors. However, the functional role of serotonin receptors in regulation of dendritic cell functions is poorly understood. Here, we demonstrate that expression of serotonin receptor 5-HT7 (5-HT 7 R) as well as its downstream effector Cdc42 is upregulated in dendritic cells upon maturation. Although dendritic cell maturation was independent of 5-HT 7 R, receptor stimulation affected dendritic cell morphology through Cdc42-mediated signaling. In addition, basal activity of 5-HT 7 R was required for the proper expression of the chemokine receptor CCR7, which is a key factor that controls dendritic cell migration. Consistent with this, we observed that 5-HT 7 R enhances chemotactic motility of dendritic cells in vitro by modulating their directionality and migration velocity. Accordingly, migration of dendritic cells in murine colon explants was abolished after pharmacological receptor inhibition. Our results indicate that there is a crucial role for 5-HT 7 R-Cdc42-mediated signaling in the regulation of dendritic cell morphology and motility, suggesting that 5-HT 7 R could be a new target for treatment of a variety of inflammatory and immune disorders.

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Section: Introductionmentioning

confidence: 99%

Serotonin receptor 5-HT7 regulates morphology and migratory properties of dendritic cells

Holst

Guseva

Schindler

et al. 2015

Journal of Cell Science

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“…For example, stem cell factor, CCL2, and TGFbeta1 are also chemotactic for mast cells (Nilsson et al, 1994;Berger et al, 2003;Collington et al, 2010). It has been demonstrated that 5-Hydroxytryptamine can induce mast cell adhesion and migration as well (Kushnir-Sukhov et al, 2006). Therefore, further work is required to identify some other important factors that may be involved in mast cells migration.…”

Section: Discussionmentioning

confidence: 99%

Distribution Change of Mast Cells in Human Nasal Polyps

Zhang

Shao

et al. 2012

The Anatomical Record

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Recent studies have shown that mast cells are involved in pathophysiologic processes of chronic inflammation. However, little is known about the distribution of mast cells in nasal polyps, which is a chronic inflammatory disease of the upper airways. Biopsy specimens from patients with nasal polyps (n ¼ 20) and control patients without nasal polyps (n ¼ 8) were included in this study. The distribution of mast cells in nasal polyps was determined by immunohistochemistry. Meanwhile, we detected the expression of chemokines (CCL5, CCL11, CX3CL1, IL-8, IL-6) in the epithelial cells of normal nasal mucosa and nasal polyps. In addition, the expression of these chemokines was investigated by western bolting in airway epithelial cells line (A549 cells) under inflammatory condition. Mast cells migrated toward intraepithelium in nasal polyps and the expression of chemokines (CCL5, CCL11, CX3CL1, IL-8) was up-regulated in the epithelial cells of nasal polyps compared with normal nasal mucosa. The expression of chemokines was also up-regulated in A549 cells after Lipopolysaccharide (LPS)-treatment for 3 hr and 6 hr. Our findings showed that mast cells migrate toward intraepithelium in nasal polyps and the overexpression of chemokines (CCL5, CCL11, CX3CL1, IL-8) suggested that they might be responsible for mast cells migration. It implies that mast cell play potential roles in the development of nasal polyps.

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“…CNG channels are functionally expressed in alveolar epithelial type II cells and may contribute to the fluid-reabsorptive driving force in the adult lung (Kemp et al, 2001). Of the mast-cell amines, the neurotransmitter 5-HT has a potential role in the pathophysiology of fibrosis (Aldenborg et al, 1993) and is implicated in enhancement of the inflammatory reactions of various organs including the lung (Kushnir-Sukhov et al, 2006). Recently, calcium ionhomeostasis was reported as having a physiological role for 5-HT and serotoninergic receptors in epithelial cells.…”

Section: Discussionmentioning

confidence: 99%

Novel and Extensive Aspects of Paraquat-Induced Pulmonary Fibrogenesis: Comparative and Time-Course Microarray Analyses in Fibrogenic and Non-Fibrogenic Rats

et al. 2007

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-Although paraquat (PQ) is widely known to induce pulmonary fibrosis, the molecular mechanisms are poorly understood. Therefore, to bring a new dimension to the elucidation of the mechanisms, we conducted microarray experiments to investigate the expression profiles of 1,090 genes in the lungs during the progressive phase of PQ-induced pulmonary fibrosis in rats. After several s.c. injections of PQ, rats were divided into a fibrogenic group and a non-fibrogenic group. Time-course gene expression analysis of the fibrogenic group showed altered gene regulation throughout the experimental period. The expression levels of many cell membrane channel, transporter, and receptor genes were substantially altered. These genes were classified into two categories: polyamine transporter-and electrolyte/fluid balance-related genes. Moreover, comparative analysis of the fibrogenic and the non-fibrogenic group revealed 36 genes with significantly different patterns of expression, including the pro-apoptotic gene Bad. This indicates that Bad is a key factor in apoptosis and that apoptosis provides a major turning point in PQ-induced pulmonary fibrosis. Notably, subtypes of transforming growth factor (TGF)-β genes that are considered to play a pivotal role in fibrogenesis showed no differences in expression between the two groups, though TGF-β3 was markedly induced in both groups. These results provide novel and extensive insights into the molecular mechanisms that lead to pulmonary fibrosis after exposure to PQ.

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5-Hydroxytryptamine Induces Mast Cell Adhesion and Migration

Cited by 131 publications

References 52 publications

Serotonin receptor 5-HT7 regulates morphology and migratory properties of dendritic cells

Serotonin receptor 5-HT7 regulates morphology and migratory properties of dendritic cells

Distribution Change of Mast Cells in Human Nasal Polyps

Novel and Extensive Aspects of Paraquat-Induced Pulmonary Fibrogenesis: Comparative and Time-Course Microarray Analyses in Fibrogenic and Non-Fibrogenic Rats

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