alexa Signaling Pathways Involved in the Effects of Different Fatty Acids on Interleukin-2 Induced Human Lymphocyte Proliferation | OMICS International | Abstract
ISSN: 2155-9899

Journal of Clinical & Cellular Immunology
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Research Article

Signaling Pathways Involved in the Effects of Different Fatty Acids on Interleukin-2 Induced Human Lymphocyte Proliferation

Renata Gorjão1,2*, Sandro M Hirabara1,2, Maria F Cury-Boaventura1, Thais Martins de Lima2, Maria Elizabeth P Passos1, Adriana C Levada-Pires1 and Rui Curi2
1Post-Graduate Program in Human Movement Sciences, Institute of Physical Activity Sciences and Sports, Cruzeiro do Sul University, Sao Paulo, Brazil
2Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Sao Paulo, Brazil
Corresponding Author : Renata Gorjão
Post-Graduate Program in Human Movement Sciences
Institute of Physical Activity Sciences and Sports
Cruzeiro do Sul University, Rua Galvão Bueno
868, Liberdade, Sao Paulo, SP, Brazil 01506-000
Tel: 55-11-3385-3103
E-mail: [email protected]
Received September 24, 2013; Accepted November 11, 2013; Published November 18, 2013
Citation: Gorjão R, Hirabara SM, Cury-Boaventura MF, de Lima TM, Passos MEP, et al. (2013) Signaling Pathways Involved in the Effects of Different Fatty Acids on Interleukin-2 Induced Human Lymphocyte Proliferation. J Clin Cell Immunol 4:171. doi:10.4172/2155-9899.1000171
Copyright: © 2013 Gorjão R, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

The aim of the present study was to investigate the mechanisms involved in the modulation of human lymphocyte proliferation by different fatty acids. We evaluated the effects of palmitic (PA), stearic (SA), oleic (OA), linoleic (LA), docosahexaenoic (DHA), and eicosapentaenoic (EPA) acids on IL-2 signaling pathways in addition to the involvement of the de novo ceramide synthesis and PI3K pathway. PA, SA, DHA, and EPA decreased the JAK1/JAK3/STAT5 pathway and IL-2-induced Akt phosphorylation. OA and LA had no effect. The inhibitory effect of DHA and EPA on lymphocyte proliferation was abolished by fumonisin B1 (FB1, an inhibitor of the de novo ceramide synthesis), whereas the effect of the other fatty acids remained unchanged. ERK1/2 phosphorylation was increased by OA and LA but markedly decreased by the other fatty acids. PKC-ζ phosphorylation was increased by OA and LA only. These effects were abolished in the presence of wortmannin, a PI3K inhibitor. In conclusion, the findings reported herein contribute for understanding the mechanisms by which different fatty acids modulate lymphocyte proliferation. The inhibitory effect of PA, SA, DHA and EPA on lymphocyte proliferation was associated with a reduction in the IL-2- mediated activation of the JAK/STAT, ERK, and Akt pathways. Decreased lymphocyte proliferation promoted by DHA and EPA also involved de novo ceramide synthesis. The stimulatory effect of OA and LA on lymphocyte proliferation was associated with improved activity of the MAP kinase and PI3K pathways, as demonstrated by increased ERK1/2 and PKC-ζ phosphorylation.

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