Sulforaphane Reduces the Chronic Inflammatory Immune Response of Human Dendritic Cells
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Published:2023-07-31
Issue:15
Volume:15
Page:3405
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ISSN:2072-6643
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Container-title:Nutrients
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language:en
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Short-container-title:Nutrients
Author:
Fernandez-Prades Laura1, Brasal-Prieto Mariano1, Alba Gonzalo1ORCID, Martin Victoria1, Montserrat-de la Paz Sergio1ORCID, Cejudo-Guillen Marta2, Santa-Maria Consuelo3ORCID, Dakhaoui Hala1ORCID, Granados Beatriz4, Sobrino Francisco1, Palomares Francisca1, Lopez-Enriquez Soledad1ORCID
Affiliation:
1. Department of Medical Biochemistry and Molecular Biology, and Immunology, School of Medicine, University of Seville, Av. Sanchez Pizjuan s/n, 41009 Seville, Spain 2. Department of Pharmacology, Pediatry, and Radiology, School of Medicine, University of Seville, Av. Sanchez Pizjuan s/n, 41009 Seville, Spain 3. Department of Biochemistry and Molecular Biology, School of Pharmacy, University of Seville, 41012 Seville, Spain 4. Distrito Sanitario Málaga, Servicio Andaluz de Salud, 29006 Málaga, Spain
Abstract
Background: Sulforaphane (SFN) is an isothiocyanate of vegetable origin with potent antioxidant and immunomodulatory properties. The characterization of its pleiotropic activity in human dendritic cells (DCs) is poorly summarized. The aim of this work was to study the immunomodulatory power of SFN in response to an inflammatory microenvironment on human monocyte-derived DCs (moDCs). Methods: We studied the immunological response induced by SFN. Apoptosis and autophagy assays were performed using flow cytometry on moDCs and a cancer cell line (THP-1). These included moDC maturation, lymphocyte proliferation and cytokine production under different experimental conditions. We investigated whether these results were associated with an inflammatory microenvironment induced by lipopolysaccharides (LPSs). Results: Our results demonstrated that SFN could interact with moDCs, significantly reducing the autophagy process and enhancing apoptosis similarly to cancer cell line THP-1 cells in a chronic inflammatory microenvironment. Under chronic inflammation, SFN modulated the phenotypical characteristics of moDCs, reducing the expression of all markers (CD80, CD83, CD86, HLA-DR and PD-L1). SFN significantly reduced the Th2 proliferative response, with a decrease in the IL-9 and IL-13 levels. Although we did not observe any changes in the regulatory proliferative response, we noted an increase in the IL-10 levels. Conclusions: These findings demonstrate that SFN exerts protective effects against LPS-induced inflammation via the modulation of moDCs/T cells towards a regulatory profile. SFN may be a potential candidate for the treatment of pathologies with an inflammatory profile.
Funder
University of Seville Ministry of Science and Innovation
Subject
Food Science,Nutrition and Dietetics
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