Effects of Antidepressants on IP-10 Production in LPS-Activated THP-1 Human Monocytes

Major depressive disorder and cardiovascular disease are common serious illnesses worldwide. Selective serotonin reuptake inhibitors and norepinephrine-dopamine reuptake inhibitors may reduce the mortality of cardiovascular disease patients with comorbid depression. Interferon-γ-inducible protein 10...

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Main Authors:	Tsai, Jui-Hsiu, Kuo, Chang-Hung, Yang, Pinchen, Cheng, Kuang-Hung, Wang, Peng-Wei, Chen, Cheng-Chung, Hung, Chih-Hsing
Format:	Online
Language:	English
Published:	MDPI 2014
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159790/

id	pubmed-4159790
recordtype	oai_dc
spelling	pubmed-41597902014-09-18 Effects of Antidepressants on IP-10 Production in LPS-Activated THP-1 Human Monocytes Tsai, Jui-Hsiu Kuo, Chang-Hung Yang, Pinchen Cheng, Kuang-Hung Wang, Peng-Wei Chen, Cheng-Chung Hung, Chih-Hsing Article Major depressive disorder and cardiovascular disease are common serious illnesses worldwide. Selective serotonin reuptake inhibitors and norepinephrine-dopamine reuptake inhibitors may reduce the mortality of cardiovascular disease patients with comorbid depression. Interferon-γ-inducible protein 10 (IP-10), a type 1 T helper cell (Th1)-related chemokine, contributes to manifestations of atherosclerosis during cardiovascular inflammations; however, the pathophysiological mechanisms linking cardiovascular disease and effective antidepressants have remained elusive. We investigated the in vitro effects of six different classes of antidepressants on the IP-10 chemokine expression in lipopolysaccharide (LPS)-stimulated monocytes, and their detailed intracellular mechanisms. The human monocytes were pretreated with antidepressants (10−8–10−5 M) before LPS-stimulation. IP-10 was measured by enzyme-linked immunosorbent assay (ELISA) and then intracellular signaling was investigated using Western blotting and chromatin immunoprecipitation. Fluoxetine and bupropion suppressed LPS-induced IP-10 expression in monocytes, and they had no cytotoxic effects. Furthermore, fluoxetine inhibited LPS-induced IP-10 expression via the mitogen-activated protein kinase (MAPK)-p38 pathway. Fluoxetine and bupropion could not only treat depression but also reduce Th1-related chemokine IP-10 production in human monocytes. Our results may indicate a possible mechanism related to how particular antidepressants reduce the risk of cardiovascular disease. MDPI 2014-07-28 /pmc/articles/PMC4159790/ /pubmed/25073092 http://dx.doi.org/10.3390/ijms150813223 Text en © 2014 by the authors; licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/).
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Tsai, Jui-Hsiu Kuo, Chang-Hung Yang, Pinchen Cheng, Kuang-Hung Wang, Peng-Wei Chen, Cheng-Chung Hung, Chih-Hsing
spellingShingle	Tsai, Jui-Hsiu Kuo, Chang-Hung Yang, Pinchen Cheng, Kuang-Hung Wang, Peng-Wei Chen, Cheng-Chung Hung, Chih-Hsing Effects of Antidepressants on IP-10 Production in LPS-Activated THP-1 Human Monocytes
author_facet	Tsai, Jui-Hsiu Kuo, Chang-Hung Yang, Pinchen Cheng, Kuang-Hung Wang, Peng-Wei Chen, Cheng-Chung Hung, Chih-Hsing
author_sort	Tsai, Jui-Hsiu
title	Effects of Antidepressants on IP-10 Production in LPS-Activated THP-1 Human Monocytes
title_short	Effects of Antidepressants on IP-10 Production in LPS-Activated THP-1 Human Monocytes
title_full	Effects of Antidepressants on IP-10 Production in LPS-Activated THP-1 Human Monocytes
title_fullStr	Effects of Antidepressants on IP-10 Production in LPS-Activated THP-1 Human Monocytes
title_full_unstemmed	Effects of Antidepressants on IP-10 Production in LPS-Activated THP-1 Human Monocytes
title_sort	effects of antidepressants on ip-10 production in lps-activated thp-1 human monocytes
description	Major depressive disorder and cardiovascular disease are common serious illnesses worldwide. Selective serotonin reuptake inhibitors and norepinephrine-dopamine reuptake inhibitors may reduce the mortality of cardiovascular disease patients with comorbid depression. Interferon-γ-inducible protein 10 (IP-10), a type 1 T helper cell (Th1)-related chemokine, contributes to manifestations of atherosclerosis during cardiovascular inflammations; however, the pathophysiological mechanisms linking cardiovascular disease and effective antidepressants have remained elusive. We investigated the in vitro effects of six different classes of antidepressants on the IP-10 chemokine expression in lipopolysaccharide (LPS)-stimulated monocytes, and their detailed intracellular mechanisms. The human monocytes were pretreated with antidepressants (10−8–10−5 M) before LPS-stimulation. IP-10 was measured by enzyme-linked immunosorbent assay (ELISA) and then intracellular signaling was investigated using Western blotting and chromatin immunoprecipitation. Fluoxetine and bupropion suppressed LPS-induced IP-10 expression in monocytes, and they had no cytotoxic effects. Furthermore, fluoxetine inhibited LPS-induced IP-10 expression via the mitogen-activated protein kinase (MAPK)-p38 pathway. Fluoxetine and bupropion could not only treat depression but also reduce Th1-related chemokine IP-10 production in human monocytes. Our results may indicate a possible mechanism related to how particular antidepressants reduce the risk of cardiovascular disease.
publisher	MDPI
publishDate	2014
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159790/
_version_	1613132601328926720

Effects of Antidepressants on IP-10 Production in LPS-Activated THP-1 Human Monocytes

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