Eicosapentaenoic acid is more effective than docosahexaenoic acid in inhibiting proinflammatory mediator production and transcription from LPS-induced human asthmatic alveolar macrophage cells

Timothy D. Mickleborough, Sandra L. Tecklenburg, Gregory Montgomery, Martin R. Lindley

Research output: Contribution to journalArticle

46 Citations (Scopus)

Abstract

Background & aims: The purpose of the study was to determine which of the active constituents of fish oil, eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), is most effective in suppressing proinflammatory mediator generation and cytokine expression from LPS-stimulated human asthmatic alveolar macrophages (AMφ). Methods: The AMφ were obtained from twenty-one asthmatic adults using fiberoptic bronchoscopy. Cells were pretreated with DMEM, pure EPA, an EPA-rich media (45% EPA/10% DHA), pure DHA, a DHA-rich media (10% EPA/50% DHA) or Lipovenos® (n-6 PUFA), and then exposed to Dulbecco's Modified Eagle's Medium (DMEM) (-) or LPS (+). Supernatants were analyzed for leukotriene (LT)B4, prostaglandin (PG)D2, tumor necrosis factor (TNF)-α and interleukin (IL)-1β production. Detection of TNF-α and IL-1β mRNA expression levels was quantified by reverse transcriptase polymerase chain reaction. Results: 120 μM pure EPA and EPA-rich media significantly (p < 0.05) suppressed TNF-α and IL-1β mRNA expression and the production of LTB4, PGD2 and TNF-α and IL-1β in LPS-stimulated primary AMφ cells obtained from asthmatic patients to a much greater extent than 120 μM pure DHA and DHA-rich media respectively. Conclusions: This study has shown for the first time that EPA is a more potent inhibitor than DHA of inflammatory responses in human asthmatic AMφ cells.

Original languageEnglish
Pages (from-to)71-77
Number of pages7
JournalClinical Nutrition
Volume28
Issue number1
DOIs
StatePublished - Feb 2009

Fingerprint

Alveolar Epithelial Cells
Eicosapentaenoic Acid
Docosahexaenoic Acids
Alveolar Macrophages
Interleukin-1
Tumor Necrosis Factor-alpha
Prostaglandin D2
Eagles
Leukotriene B4
Messenger RNA
Fish Oils
Bronchoscopy
Reverse Transcriptase Polymerase Chain Reaction
Cytokines

Keywords

  • Asthma
  • Docohexaenoic acid
  • Eicosapentaenoic acid
  • Fish oil
  • Proinflammatory mediators

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine
  • Nutrition and Dietetics

Cite this

Eicosapentaenoic acid is more effective than docosahexaenoic acid in inhibiting proinflammatory mediator production and transcription from LPS-induced human asthmatic alveolar macrophage cells. / Mickleborough, Timothy D.; Tecklenburg, Sandra L.; Montgomery, Gregory; Lindley, Martin R.

In: Clinical Nutrition, Vol. 28, No. 1, 02.2009, p. 71-77.

Research output: Contribution to journalArticle

@article{c944f45ff944433f9ab77cbb759d2f43,
title = "Eicosapentaenoic acid is more effective than docosahexaenoic acid in inhibiting proinflammatory mediator production and transcription from LPS-induced human asthmatic alveolar macrophage cells",
abstract = "Background & aims: The purpose of the study was to determine which of the active constituents of fish oil, eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), is most effective in suppressing proinflammatory mediator generation and cytokine expression from LPS-stimulated human asthmatic alveolar macrophages (AMφ). Methods: The AMφ were obtained from twenty-one asthmatic adults using fiberoptic bronchoscopy. Cells were pretreated with DMEM, pure EPA, an EPA-rich media (45{\%} EPA/10{\%} DHA), pure DHA, a DHA-rich media (10{\%} EPA/50{\%} DHA) or Lipovenos{\circledR} (n-6 PUFA), and then exposed to Dulbecco's Modified Eagle's Medium (DMEM) (-) or LPS (+). Supernatants were analyzed for leukotriene (LT)B4, prostaglandin (PG)D2, tumor necrosis factor (TNF)-α and interleukin (IL)-1β production. Detection of TNF-α and IL-1β mRNA expression levels was quantified by reverse transcriptase polymerase chain reaction. Results: 120 μM pure EPA and EPA-rich media significantly (p < 0.05) suppressed TNF-α and IL-1β mRNA expression and the production of LTB4, PGD2 and TNF-α and IL-1β in LPS-stimulated primary AMφ cells obtained from asthmatic patients to a much greater extent than 120 μM pure DHA and DHA-rich media respectively. Conclusions: This study has shown for the first time that EPA is a more potent inhibitor than DHA of inflammatory responses in human asthmatic AMφ cells.",
keywords = "Asthma, Docohexaenoic acid, Eicosapentaenoic acid, Fish oil, Proinflammatory mediators",
author = "Mickleborough, {Timothy D.} and Tecklenburg, {Sandra L.} and Gregory Montgomery and Lindley, {Martin R.}",
year = "2009",
month = "2",
doi = "10.1016/j.clnu.2008.10.012",
language = "English",
volume = "28",
pages = "71--77",
journal = "Clinical Nutrition",
issn = "0261-5614",
publisher = "Churchill Livingstone",
number = "1",

}

TY - JOUR

T1 - Eicosapentaenoic acid is more effective than docosahexaenoic acid in inhibiting proinflammatory mediator production and transcription from LPS-induced human asthmatic alveolar macrophage cells

AU - Mickleborough, Timothy D.

AU - Tecklenburg, Sandra L.

AU - Montgomery, Gregory

AU - Lindley, Martin R.

PY - 2009/2

Y1 - 2009/2

N2 - Background & aims: The purpose of the study was to determine which of the active constituents of fish oil, eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), is most effective in suppressing proinflammatory mediator generation and cytokine expression from LPS-stimulated human asthmatic alveolar macrophages (AMφ). Methods: The AMφ were obtained from twenty-one asthmatic adults using fiberoptic bronchoscopy. Cells were pretreated with DMEM, pure EPA, an EPA-rich media (45% EPA/10% DHA), pure DHA, a DHA-rich media (10% EPA/50% DHA) or Lipovenos® (n-6 PUFA), and then exposed to Dulbecco's Modified Eagle's Medium (DMEM) (-) or LPS (+). Supernatants were analyzed for leukotriene (LT)B4, prostaglandin (PG)D2, tumor necrosis factor (TNF)-α and interleukin (IL)-1β production. Detection of TNF-α and IL-1β mRNA expression levels was quantified by reverse transcriptase polymerase chain reaction. Results: 120 μM pure EPA and EPA-rich media significantly (p < 0.05) suppressed TNF-α and IL-1β mRNA expression and the production of LTB4, PGD2 and TNF-α and IL-1β in LPS-stimulated primary AMφ cells obtained from asthmatic patients to a much greater extent than 120 μM pure DHA and DHA-rich media respectively. Conclusions: This study has shown for the first time that EPA is a more potent inhibitor than DHA of inflammatory responses in human asthmatic AMφ cells.

AB - Background & aims: The purpose of the study was to determine which of the active constituents of fish oil, eicosapentaenoic acid (EPA) or docosahexaenoic acid (DHA), is most effective in suppressing proinflammatory mediator generation and cytokine expression from LPS-stimulated human asthmatic alveolar macrophages (AMφ). Methods: The AMφ were obtained from twenty-one asthmatic adults using fiberoptic bronchoscopy. Cells were pretreated with DMEM, pure EPA, an EPA-rich media (45% EPA/10% DHA), pure DHA, a DHA-rich media (10% EPA/50% DHA) or Lipovenos® (n-6 PUFA), and then exposed to Dulbecco's Modified Eagle's Medium (DMEM) (-) or LPS (+). Supernatants were analyzed for leukotriene (LT)B4, prostaglandin (PG)D2, tumor necrosis factor (TNF)-α and interleukin (IL)-1β production. Detection of TNF-α and IL-1β mRNA expression levels was quantified by reverse transcriptase polymerase chain reaction. Results: 120 μM pure EPA and EPA-rich media significantly (p < 0.05) suppressed TNF-α and IL-1β mRNA expression and the production of LTB4, PGD2 and TNF-α and IL-1β in LPS-stimulated primary AMφ cells obtained from asthmatic patients to a much greater extent than 120 μM pure DHA and DHA-rich media respectively. Conclusions: This study has shown for the first time that EPA is a more potent inhibitor than DHA of inflammatory responses in human asthmatic AMφ cells.

KW - Asthma

KW - Docohexaenoic acid

KW - Eicosapentaenoic acid

KW - Fish oil

KW - Proinflammatory mediators

UR - http://www.scopus.com/inward/record.url?scp=59149096364&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=59149096364&partnerID=8YFLogxK

U2 - 10.1016/j.clnu.2008.10.012

DO - 10.1016/j.clnu.2008.10.012

M3 - Article

VL - 28

SP - 71

EP - 77

JO - Clinical Nutrition

JF - Clinical Nutrition

SN - 0261-5614

IS - 1

ER -