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Immunostimulatory activity of fluoxetine in macrophages via regulation of the PI3K and P38 signaling pathways
Fluoxetine is an antidepressant drug that is heavily preferred in the cure of depression, which is from the selective serotonin reuptake inhibitor (SSRI) group. There are many reports on the effect of fluoxetine on the immune system, and its effect on the macrophage cells has never been looked at be...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Springer US
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9745289/ https://www.ncbi.nlm.nih.gov/pubmed/36512200 http://dx.doi.org/10.1007/s12026-022-09350-4 |
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author | Önal, Harika Topal Yetkin, Derya Ayaz, Furkan |
author_facet | Önal, Harika Topal Yetkin, Derya Ayaz, Furkan |
author_sort | Önal, Harika Topal |
collection | PubMed |
description | Fluoxetine is an antidepressant drug that is heavily preferred in the cure of depression, which is from the selective serotonin reuptake inhibitor (SSRI) group. There are many reports on the effect of fluoxetine on the immune system, and its effect on the macrophage cells has never been looked at before. We aimed to demonstrate the cytokine production potential of fluoxetine antidepressant, which is widely used in the clinic, in the J774.2 cell line and its effect on PI3K and P38 pathways. The use of fluoxetine alone in J774.2 macrophage cells showed immunostimulatory properties by inducing the production of tumor necrosis factor-α (TNF-α), interleukin (IL) IL-6, IL-12p40, and granulocyte–macrophage colony-stimulating factor (GM-CSF) cytokines. It showed anti-inflammatory properties by completely stopping the production of cytokines (IL-6, IL12p40, TNF-α, and GM-CSF) at all concentrations where LPS and fluoxetine were used together. While PI3K and P38 pathways were not effective in the immunostimulatory effect in the presence of the drug agent, we found that the PI3K and P38 pathways were influenced during their anti-inflammatory activity. |
format | Online Article Text |
id | pubmed-9745289 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Springer US |
record_format | MEDLINE/PubMed |
spelling | pubmed-97452892022-12-13 Immunostimulatory activity of fluoxetine in macrophages via regulation of the PI3K and P38 signaling pathways Önal, Harika Topal Yetkin, Derya Ayaz, Furkan Immunol Res Original Article Fluoxetine is an antidepressant drug that is heavily preferred in the cure of depression, which is from the selective serotonin reuptake inhibitor (SSRI) group. There are many reports on the effect of fluoxetine on the immune system, and its effect on the macrophage cells has never been looked at before. We aimed to demonstrate the cytokine production potential of fluoxetine antidepressant, which is widely used in the clinic, in the J774.2 cell line and its effect on PI3K and P38 pathways. The use of fluoxetine alone in J774.2 macrophage cells showed immunostimulatory properties by inducing the production of tumor necrosis factor-α (TNF-α), interleukin (IL) IL-6, IL-12p40, and granulocyte–macrophage colony-stimulating factor (GM-CSF) cytokines. It showed anti-inflammatory properties by completely stopping the production of cytokines (IL-6, IL12p40, TNF-α, and GM-CSF) at all concentrations where LPS and fluoxetine were used together. While PI3K and P38 pathways were not effective in the immunostimulatory effect in the presence of the drug agent, we found that the PI3K and P38 pathways were influenced during their anti-inflammatory activity. Springer US 2022-12-13 2023 /pmc/articles/PMC9745289/ /pubmed/36512200 http://dx.doi.org/10.1007/s12026-022-09350-4 Text en © The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022, Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law. This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic. |
spellingShingle | Original Article Önal, Harika Topal Yetkin, Derya Ayaz, Furkan Immunostimulatory activity of fluoxetine in macrophages via regulation of the PI3K and P38 signaling pathways |
title | Immunostimulatory activity of fluoxetine in macrophages via regulation of the PI3K and P38 signaling pathways |
title_full | Immunostimulatory activity of fluoxetine in macrophages via regulation of the PI3K and P38 signaling pathways |
title_fullStr | Immunostimulatory activity of fluoxetine in macrophages via regulation of the PI3K and P38 signaling pathways |
title_full_unstemmed | Immunostimulatory activity of fluoxetine in macrophages via regulation of the PI3K and P38 signaling pathways |
title_short | Immunostimulatory activity of fluoxetine in macrophages via regulation of the PI3K and P38 signaling pathways |
title_sort | immunostimulatory activity of fluoxetine in macrophages via regulation of the pi3k and p38 signaling pathways |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9745289/ https://www.ncbi.nlm.nih.gov/pubmed/36512200 http://dx.doi.org/10.1007/s12026-022-09350-4 |
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