Fluoxetine directly counteracts the adverse effects of chronic stress on T cell immunity by compensatory and specific mechanisms

Chronic stress and depression are widely known to down-regulate the immune system, and several antidepressants can reverse this impairment, with or without effects in normal subjects. Although the central nervous system is undoubtedly involved in these events, some psychotropic drugs can also exert...

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Publicado: 2009
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Acceso en línea:https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_08891591_v23_n1_p36_Frick
http://hdl.handle.net/20.500.12110/paper_08891591_v23_n1_p36_Frick
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spelling paper:paper_08891591_v23_n1_p36_Frick2023-06-08T15:47:03Z Fluoxetine directly counteracts the adverse effects of chronic stress on T cell immunity by compensatory and specific mechanisms Antidepressant B cells CD4/CD8 Chronic stress Cytokines Depression Fluoxetine Natural killer T cells concanavalin A fluoxetine gamma interferon interleukin 2 tumor necrosis factor alpha animal cell animal experiment animal model animal tissue article CD4 CD8 ratio cell proliferation cellular immunity chronic stress controlled study depression drug mechanism female in vitro study nonhuman priority journal T lymphocyte Animals Antidepressive Agents, Second-Generation B-Lymphocytes CD4-CD8 Ratio CD4-Positive T-Lymphocytes CD8-Positive T-Lymphocytes Cell Proliferation Chronic Disease Female Flow Cytometry Fluoxetine Interferon-gamma Interleukin-2 Killer Cells, Natural Mice Mice, Inbred BALB C Restraint, Physical Reverse Transcriptase Polymerase Chain Reaction Stress, Psychological T-Lymphocytes Tumor Necrosis Factor-alpha Chronic stress and depression are widely known to down-regulate the immune system, and several antidepressants can reverse this impairment, with or without effects in normal subjects. Although the central nervous system is undoubtedly involved in these events, some psychotropic drugs can also exert direct effects on lymphoid cells. We have recently shown that the antidepressant fluoxetine enhances T cell proliferation and TH1 cytokine production in vivo, without changes on CD4/CD8 subsets. In vitro, a direct action of fluoxetine upon T lymphocyte reactivity by complex mechanisms was also described. In another work, we also found that chronic stress reduces T cell mediated immunity, namely a decrease of T cell response to mitogens, TH1 cytokine production and CD4+-but not CD8+-T lymphocytes. Here we investigated the effects of fluoxetine on chronic stress-driven immune system depression. We found that fluoxetine restored T cell proliferation and interleukin-2, interferon-γ and tumor necrosis factor-α production by compensatory mechanisms. In addition, CD4/CD8 ratio was also normalized by antidepressant administration, but this seems to be a non-compensatory effect associated specifically to stress. No changes were observed in other lymphoid cells, i.e. natural killer cells and B lymphocytes. Finally, we observed that fluoxetine is able to reverse T cell reactivity impairment in vitro by a direct action at clinically relevant doses. These results highlight the relevance of pharmacological treatment of stress and depression, and may help to begin elucidating the complex events triggered-directly and/or indirectly-by antidepressants in non-neuronal cell types. © 2008 Elsevier Inc. All rights reserved. 2009 https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_08891591_v23_n1_p36_Frick http://hdl.handle.net/20.500.12110/paper_08891591_v23_n1_p36_Frick
institution Universidad de Buenos Aires
institution_str I-28
repository_str R-134
collection Biblioteca Digital - Facultad de Ciencias Exactas y Naturales (UBA)
topic Antidepressant
B cells
CD4/CD8
Chronic stress
Cytokines
Depression
Fluoxetine
Natural killer
T cells
concanavalin A
fluoxetine
gamma interferon
interleukin 2
tumor necrosis factor alpha
animal cell
animal experiment
animal model
animal tissue
article
CD4 CD8 ratio
cell proliferation
cellular immunity
chronic stress
controlled study
depression
drug mechanism
female
in vitro study
nonhuman
priority journal
T lymphocyte
Animals
Antidepressive Agents, Second-Generation
B-Lymphocytes
CD4-CD8 Ratio
CD4-Positive T-Lymphocytes
CD8-Positive T-Lymphocytes
Cell Proliferation
Chronic Disease
Female
Flow Cytometry
Fluoxetine
Interferon-gamma
Interleukin-2
Killer Cells, Natural
Mice
Mice, Inbred BALB C
Restraint, Physical
Reverse Transcriptase Polymerase Chain Reaction
Stress, Psychological
T-Lymphocytes
Tumor Necrosis Factor-alpha
spellingShingle Antidepressant
B cells
CD4/CD8
Chronic stress
Cytokines
Depression
Fluoxetine
Natural killer
T cells
concanavalin A
fluoxetine
gamma interferon
interleukin 2
tumor necrosis factor alpha
animal cell
animal experiment
animal model
animal tissue
article
CD4 CD8 ratio
cell proliferation
cellular immunity
chronic stress
controlled study
depression
drug mechanism
female
in vitro study
nonhuman
priority journal
T lymphocyte
Animals
Antidepressive Agents, Second-Generation
B-Lymphocytes
CD4-CD8 Ratio
CD4-Positive T-Lymphocytes
CD8-Positive T-Lymphocytes
Cell Proliferation
Chronic Disease
Female
Flow Cytometry
Fluoxetine
Interferon-gamma
Interleukin-2
Killer Cells, Natural
Mice
Mice, Inbred BALB C
Restraint, Physical
Reverse Transcriptase Polymerase Chain Reaction
Stress, Psychological
T-Lymphocytes
Tumor Necrosis Factor-alpha
Fluoxetine directly counteracts the adverse effects of chronic stress on T cell immunity by compensatory and specific mechanisms
topic_facet Antidepressant
B cells
CD4/CD8
Chronic stress
Cytokines
Depression
Fluoxetine
Natural killer
T cells
concanavalin A
fluoxetine
gamma interferon
interleukin 2
tumor necrosis factor alpha
animal cell
animal experiment
animal model
animal tissue
article
CD4 CD8 ratio
cell proliferation
cellular immunity
chronic stress
controlled study
depression
drug mechanism
female
in vitro study
nonhuman
priority journal
T lymphocyte
Animals
Antidepressive Agents, Second-Generation
B-Lymphocytes
CD4-CD8 Ratio
CD4-Positive T-Lymphocytes
CD8-Positive T-Lymphocytes
Cell Proliferation
Chronic Disease
Female
Flow Cytometry
Fluoxetine
Interferon-gamma
Interleukin-2
Killer Cells, Natural
Mice
Mice, Inbred BALB C
Restraint, Physical
Reverse Transcriptase Polymerase Chain Reaction
Stress, Psychological
T-Lymphocytes
Tumor Necrosis Factor-alpha
description Chronic stress and depression are widely known to down-regulate the immune system, and several antidepressants can reverse this impairment, with or without effects in normal subjects. Although the central nervous system is undoubtedly involved in these events, some psychotropic drugs can also exert direct effects on lymphoid cells. We have recently shown that the antidepressant fluoxetine enhances T cell proliferation and TH1 cytokine production in vivo, without changes on CD4/CD8 subsets. In vitro, a direct action of fluoxetine upon T lymphocyte reactivity by complex mechanisms was also described. In another work, we also found that chronic stress reduces T cell mediated immunity, namely a decrease of T cell response to mitogens, TH1 cytokine production and CD4+-but not CD8+-T lymphocytes. Here we investigated the effects of fluoxetine on chronic stress-driven immune system depression. We found that fluoxetine restored T cell proliferation and interleukin-2, interferon-γ and tumor necrosis factor-α production by compensatory mechanisms. In addition, CD4/CD8 ratio was also normalized by antidepressant administration, but this seems to be a non-compensatory effect associated specifically to stress. No changes were observed in other lymphoid cells, i.e. natural killer cells and B lymphocytes. Finally, we observed that fluoxetine is able to reverse T cell reactivity impairment in vitro by a direct action at clinically relevant doses. These results highlight the relevance of pharmacological treatment of stress and depression, and may help to begin elucidating the complex events triggered-directly and/or indirectly-by antidepressants in non-neuronal cell types. © 2008 Elsevier Inc. All rights reserved.
title Fluoxetine directly counteracts the adverse effects of chronic stress on T cell immunity by compensatory and specific mechanisms
title_short Fluoxetine directly counteracts the adverse effects of chronic stress on T cell immunity by compensatory and specific mechanisms
title_full Fluoxetine directly counteracts the adverse effects of chronic stress on T cell immunity by compensatory and specific mechanisms
title_fullStr Fluoxetine directly counteracts the adverse effects of chronic stress on T cell immunity by compensatory and specific mechanisms
title_full_unstemmed Fluoxetine directly counteracts the adverse effects of chronic stress on T cell immunity by compensatory and specific mechanisms
title_sort fluoxetine directly counteracts the adverse effects of chronic stress on t cell immunity by compensatory and specific mechanisms
publishDate 2009
url https://bibliotecadigital.exactas.uba.ar/collection/paper/document/paper_08891591_v23_n1_p36_Frick
http://hdl.handle.net/20.500.12110/paper_08891591_v23_n1_p36_Frick
_version_ 1768544508433137664