Eicosapentaenoic acid suppression of systemic inflammatory responses and inverse up-regulation of 15-deoxy Δ12,14 Prostaglandin J2 production

Jillian Davidson, Warren Higgs, D Rotondo

Research output: Contribution to journalArticle

5 Citations (Scopus)

Abstract

Eicosapentaenoic acid (EPA) has been shown to suppress immune cell responses, such as cytokine production and downstream PG production in vitro. Studies in vivo, however, have used EPA as a minor constituent of fish oil with variable results. We investigated the effects of EPA on systemic inflammatory responses as pure EPA has not been evaluated on immune/inflammatory responses in vivo.
Rabbits were administered polyinosinic: polycytidylic acid (poly I:C) i.v. before and after oral treatment with EPA for 42 days (given daily). The responses to IL-1β and TNF-α were also studied. Immediately following administration of poly I:C, body temperature was continuously monitored and blood samples were taken. Plasma levels of IL-1β, PGE2 (PGE2 ), and 15-deoxy-Δ(12,14) -PGJ2 (15d-PGJ2 ) were measured by enzyme immunoassay.
Following EPA treatment, the fever response to poly I:C was markedly suppressed compared with pretreatment responses. This was accompanied by a parallel reduction in the poly I:C-stimulated elevation in plasma levels of IL-1β and PGE2 . Paradoxically, the levels of 15d-PGJ2 were higher following EPA treatment. EPA treatment did not significantly alter the fever response or plasma levels of PGE2 in response to either IL-1β or TNF-α.
Oral treatment with EPA can suppress immune/inflammatory responses in vivo via a suppression of upstream cytokine production resulting in a decreased fever response and indirectly reducing circulating levels of PGE2 . EPA also enhances the production of the cytoprotective prostanoid 15d-PGJ2 indicating the therapeutic benefit of EPA.

LanguageEnglish
Pages1130-1139
Number of pages10
JournalBritish Journal of Pharmacology
Volume169
Issue number5
Early online date12 Jun 2013
DOIs
Publication statusPublished - 1 Jul 2013

Fingerprint

Eicosapentaenoic Acid
Up-Regulation
Dinoprostone
Poly I-C
Fever
9-deoxy-delta-9-prostaglandin D2
Therapeutics
Tumor Necrosis Factor-alpha
Cytokines
Fish Oils
Body Temperature
Immunoenzyme Techniques
Prostaglandins
Rabbits

Keywords

  • eicosapentaenoic acid
  • Inflammation
  • PGE2
  • 15d-PGJ(2)

Cite this

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abstract = "Eicosapentaenoic acid (EPA) has been shown to suppress immune cell responses, such as cytokine production and downstream PG production in vitro. Studies in vivo, however, have used EPA as a minor constituent of fish oil with variable results. We investigated the effects of EPA on systemic inflammatory responses as pure EPA has not been evaluated on immune/inflammatory responses in vivo. Rabbits were administered polyinosinic: polycytidylic acid (poly I:C) i.v. before and after oral treatment with EPA for 42 days (given daily). The responses to IL-1β and TNF-α were also studied. Immediately following administration of poly I:C, body temperature was continuously monitored and blood samples were taken. Plasma levels of IL-1β, PGE2 (PGE2 ), and 15-deoxy-Δ(12,14) -PGJ2 (15d-PGJ2 ) were measured by enzyme immunoassay. Following EPA treatment, the fever response to poly I:C was markedly suppressed compared with pretreatment responses. This was accompanied by a parallel reduction in the poly I:C-stimulated elevation in plasma levels of IL-1β and PGE2 . Paradoxically, the levels of 15d-PGJ2 were higher following EPA treatment. EPA treatment did not significantly alter the fever response or plasma levels of PGE2 in response to either IL-1β or TNF-α. Oral treatment with EPA can suppress immune/inflammatory responses in vivo via a suppression of upstream cytokine production resulting in a decreased fever response and indirectly reducing circulating levels of PGE2 . EPA also enhances the production of the cytoprotective prostanoid 15d-PGJ2 indicating the therapeutic benefit of EPA.",
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Eicosapentaenoic acid suppression of systemic inflammatory responses and inverse up-regulation of 15-deoxy Δ12,14 Prostaglandin J2 production. / Davidson, Jillian; Higgs, Warren; Rotondo, D.

In: British Journal of Pharmacology, Vol. 169, No. 5, 01.07.2013, p. 1130-1139.

Research output: Contribution to journalArticle

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AB - Eicosapentaenoic acid (EPA) has been shown to suppress immune cell responses, such as cytokine production and downstream PG production in vitro. Studies in vivo, however, have used EPA as a minor constituent of fish oil with variable results. We investigated the effects of EPA on systemic inflammatory responses as pure EPA has not been evaluated on immune/inflammatory responses in vivo. Rabbits were administered polyinosinic: polycytidylic acid (poly I:C) i.v. before and after oral treatment with EPA for 42 days (given daily). The responses to IL-1β and TNF-α were also studied. Immediately following administration of poly I:C, body temperature was continuously monitored and blood samples were taken. Plasma levels of IL-1β, PGE2 (PGE2 ), and 15-deoxy-Δ(12,14) -PGJ2 (15d-PGJ2 ) were measured by enzyme immunoassay. Following EPA treatment, the fever response to poly I:C was markedly suppressed compared with pretreatment responses. This was accompanied by a parallel reduction in the poly I:C-stimulated elevation in plasma levels of IL-1β and PGE2 . Paradoxically, the levels of 15d-PGJ2 were higher following EPA treatment. EPA treatment did not significantly alter the fever response or plasma levels of PGE2 in response to either IL-1β or TNF-α. Oral treatment with EPA can suppress immune/inflammatory responses in vivo via a suppression of upstream cytokine production resulting in a decreased fever response and indirectly reducing circulating levels of PGE2 . EPA also enhances the production of the cytoprotective prostanoid 15d-PGJ2 indicating the therapeutic benefit of EPA.

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