Fluoxetine augments Natural Killer (NK) cell activity in vitro: Modulation by the 5-HT1a antagonist pindobind

M. Frank, D. Johnson, S. Hendricks, J. Wieseler

Research output: Contribution to journalArticle

Abstract

Serotonin (5-HT) augments NK cell activity (NKCA) in vitro. NKCA is a component of the innate immune response to viral infection and certain tumor cells. Further, 5-HT1a receptor agonists bolster NKCA in vitro. In addition, studies suggest that lymphocytes express 5-HT reuptake transport proteins. In light of these reports, NK cells were treated with the selective serotonin reuptake inhibitor (SSRI) fluoxetine and/or the S-HT1a antagonist pindobind to further characterize serotonergic modulation of NKCA. Mononuclear cells, isolated from human blood, were incubated with drug and a standard 51chromium-release assay performed with K562 target cells. A 4 hr cytotoxicity assay was conducted and NKCA quantified as lytic units 5-HT, a 5-HT1a receptor agonist (8-OH-DPAT), and fluoxetine augmented NKCA whereas pindobind suppressed NKCA and abrogated the augmenting effects of fluoxetine. The present results provide further evidence of serotonergic modulation of NKCA through the 5-HT1a receptor and suggest a potentially important role for serotonergic agents such as SSRIs in the clinical regulation of immune function.

Original languageEnglish (US)
Pages (from-to)A905
JournalFASEB Journal
Volume12
Issue number5
StatePublished - Mar 20 1998

Fingerprint

Fluoxetine
natural killer cells
Natural Killer Cells
antagonists
Serotonin
Modulation
serotonin
Assays
Serotonin Agents
8-Hydroxy-2-(di-n-propylamino)tetralin
Lymphocytes
Serotonin Uptake Inhibitors
Cytotoxicity
Tumors
Carrier Proteins
receptors
agonists
Blood
Cells
pindobind

ASJC Scopus subject areas

  • Biotechnology
  • Biochemistry
  • Molecular Biology
  • Genetics

Cite this

Fluoxetine augments Natural Killer (NK) cell activity in vitro : Modulation by the 5-HT1a antagonist pindobind. / Frank, M.; Johnson, D.; Hendricks, S.; Wieseler, J.

In: FASEB Journal, Vol. 12, No. 5, 20.03.1998, p. A905.

Research output: Contribution to journalArticle

Frank, M, Johnson, D, Hendricks, S & Wieseler, J 1998, 'Fluoxetine augments Natural Killer (NK) cell activity in vitro: Modulation by the 5-HT1a antagonist pindobind', FASEB Journal, vol. 12, no. 5, pp. A905.
Frank, M. ; Johnson, D. ; Hendricks, S. ; Wieseler, J. / Fluoxetine augments Natural Killer (NK) cell activity in vitro : Modulation by the 5-HT1a antagonist pindobind. In: FASEB Journal. 1998 ; Vol. 12, No. 5. pp. A905.
@article{90ebc24e88b64a72a375c3b494bfaa05,
title = "Fluoxetine augments Natural Killer (NK) cell activity in vitro: Modulation by the 5-HT1a antagonist pindobind",
abstract = "Serotonin (5-HT) augments NK cell activity (NKCA) in vitro. NKCA is a component of the innate immune response to viral infection and certain tumor cells. Further, 5-HT1a receptor agonists bolster NKCA in vitro. In addition, studies suggest that lymphocytes express 5-HT reuptake transport proteins. In light of these reports, NK cells were treated with the selective serotonin reuptake inhibitor (SSRI) fluoxetine and/or the S-HT1a antagonist pindobind to further characterize serotonergic modulation of NKCA. Mononuclear cells, isolated from human blood, were incubated with drug and a standard 51chromium-release assay performed with K562 target cells. A 4 hr cytotoxicity assay was conducted and NKCA quantified as lytic units 5-HT, a 5-HT1a receptor agonist (8-OH-DPAT), and fluoxetine augmented NKCA whereas pindobind suppressed NKCA and abrogated the augmenting effects of fluoxetine. The present results provide further evidence of serotonergic modulation of NKCA through the 5-HT1a receptor and suggest a potentially important role for serotonergic agents such as SSRIs in the clinical regulation of immune function.",
author = "M. Frank and D. Johnson and S. Hendricks and J. Wieseler",
year = "1998",
month = "3",
day = "20",
language = "English (US)",
volume = "12",
pages = "A905",
journal = "FASEB Journal",
issn = "0892-6638",
publisher = "FASEB",
number = "5",

}

TY - JOUR

T1 - Fluoxetine augments Natural Killer (NK) cell activity in vitro

T2 - Modulation by the 5-HT1a antagonist pindobind

AU - Frank, M.

AU - Johnson, D.

AU - Hendricks, S.

AU - Wieseler, J.

PY - 1998/3/20

Y1 - 1998/3/20

N2 - Serotonin (5-HT) augments NK cell activity (NKCA) in vitro. NKCA is a component of the innate immune response to viral infection and certain tumor cells. Further, 5-HT1a receptor agonists bolster NKCA in vitro. In addition, studies suggest that lymphocytes express 5-HT reuptake transport proteins. In light of these reports, NK cells were treated with the selective serotonin reuptake inhibitor (SSRI) fluoxetine and/or the S-HT1a antagonist pindobind to further characterize serotonergic modulation of NKCA. Mononuclear cells, isolated from human blood, were incubated with drug and a standard 51chromium-release assay performed with K562 target cells. A 4 hr cytotoxicity assay was conducted and NKCA quantified as lytic units 5-HT, a 5-HT1a receptor agonist (8-OH-DPAT), and fluoxetine augmented NKCA whereas pindobind suppressed NKCA and abrogated the augmenting effects of fluoxetine. The present results provide further evidence of serotonergic modulation of NKCA through the 5-HT1a receptor and suggest a potentially important role for serotonergic agents such as SSRIs in the clinical regulation of immune function.

AB - Serotonin (5-HT) augments NK cell activity (NKCA) in vitro. NKCA is a component of the innate immune response to viral infection and certain tumor cells. Further, 5-HT1a receptor agonists bolster NKCA in vitro. In addition, studies suggest that lymphocytes express 5-HT reuptake transport proteins. In light of these reports, NK cells were treated with the selective serotonin reuptake inhibitor (SSRI) fluoxetine and/or the S-HT1a antagonist pindobind to further characterize serotonergic modulation of NKCA. Mononuclear cells, isolated from human blood, were incubated with drug and a standard 51chromium-release assay performed with K562 target cells. A 4 hr cytotoxicity assay was conducted and NKCA quantified as lytic units 5-HT, a 5-HT1a receptor agonist (8-OH-DPAT), and fluoxetine augmented NKCA whereas pindobind suppressed NKCA and abrogated the augmenting effects of fluoxetine. The present results provide further evidence of serotonergic modulation of NKCA through the 5-HT1a receptor and suggest a potentially important role for serotonergic agents such as SSRIs in the clinical regulation of immune function.

UR - http://www.scopus.com/inward/record.url?scp=33749271713&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33749271713&partnerID=8YFLogxK

M3 - Article

AN - SCOPUS:33749271713

VL - 12

SP - A905

JO - FASEB Journal

JF - FASEB Journal

SN - 0892-6638

IS - 5

ER -