title: Eicosapentaenoic (EPA) and docosahexaenoic (DHA) acid differentially modulate rat neutrophil function in vitro.
abstract: Fish oils are used as therapeutic agents in chronic inflammatory diseases. The omega-3 fatty acids (FA) found in these oils are mainly eicosapentaenoic (EPA) and docosahexaenoic (DHA) acids. The anti-inflammatory properties of fish oils are attributed to both omega-3 fatty acids. However, it is unknown whether such effects are due to either EPA or DHA. In this study, the effects of EPA and DHA on rat neutrophil function in vitro were compared. Both EPA and DHA increased the production of H₂O₂ when cells were stimulated or not with lipopolysaccharides (LPS). However, EPA was more potent than DHA in triggering an increase in superoxide release by cells in the basal condition or when stimulated with phorbol myristate acetate (PMA) or zymosan. Only DHA increased the phagocytic capacity and fungicidal activity of neutrophils. Both FA increased the release of tumor necrosis factor-α (TNF-α) in nonstimulated cells, but only EPA increased the production of cytokine-inducing neutrophil chemoattractant-2 (CINC-2) in the absence or presence of LPS, whereas production of interleukin-1 beta (IL-1β) was only increased by DHA in the presence of LPS. In addition, there was no alteration in the production of nitric oxide. In conclusion, we show herein that EPA and DHA can differently modulate aspects of the neutrophil response, which may be relevant for the development of therapies rich in one or other FA depending on the effect required.
authors.affiliation: Department of Physiology and Biophysics, Institute of Biomedical Sciences, University of Sao Paulo, Av. Prof. Lineu Prestes 1524, 1° Andar, Sala 105 Cidade Universitária, Sao Paulo, SP, CEP 05508-000, Brazil. vivianpaschoal@hotmail.com
authors.forename: V A
authors.initials: VA
authors.lastname: Paschoal
authors.forename: M A R
authors.initials: MA
authors.lastname: Vinolo
authors.forename: A R
authors.initials: AR
authors.lastname: Crisma
authors.forename: J
authors.initials: J
authors.lastname: Magdalon
authors.forename: R
authors.initials: R
authors.lastname: Curi
mesh_terms: D000818:Animals; D000893:Anti-Inflammatory Agents / Q000494:pharmacology*; D000935:Antifungal Agents / Q000494:pharmacology; D002176:Candida albicans / Q000187:drug effects; D002177:Candidiasis / Q000188:drug therapy; D002478:Cells, Cultured; D019743:Chemokines, CXC / Q000276:immunology; D004281:Docosahexaenoic Acids / Q000494:pharmacology*; D015118:Eicosapentaenoic Acid / Q000494:pharmacology*; D006861:Hydrogen Peroxide / Q000276:immunology; D053583:Interleukin-1beta / Q000276:immunology; D008070:Lipopolysaccharides / Q000276:immunology; D008297:Male; D009504:Neutrophils / Q000166:cytology / Q000187:drug effects* / Q000276:immunology* / Q000382:microbiology; D009569:Nitric Oxide / Q000276:immunology; D010587:Phagocytosis / Q000187:drug effects; D051381:Rats; D017208:Rats, Wistar; D017382:Reactive Oxygen Species / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology
chemical_list: D000893:Anti-Inflammatory Agents; D000935:Antifungal Agents; D019743:Chemokines, CXC; C513294:Cxcl3 protein, rat; D053583:Interleukin-1beta; D008070:Lipopolysaccharides; D017382:Reactive Oxygen Species; D014409:Tumor Necrosis Factor-alpha; D004281:Docosahexaenoic Acids; D009569:Nitric Oxide; D015118:Eicosapentaenoic Acid; D006861:Hydrogen Peroxide