Reduced lipoxygenase and cyclooxygenase mediated signaling in PBMC of atopic dermatitis patients

Johanna Mihály, Janine Gericke, Dániel Törocsik, Krisztián Gáspár, Andrea Szegedi, Ralph Rühl

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Lipoxygenases (LOX) and cyclooxygenases (COX) are the main enzymes for poly-unsaturated fatty acid (PUFA) metabolism to highly bioactive prostaglandins, leukotrienes, thromboxanes and protectins. LOX and COX pathways are highly important for the regulation of pro-and anti-inflammatory active metabolite synthesis and metabolism in various inflammatory diseases like atopic diseases (AD). In this study using QRT-PCR, we found that in PBMCs the expression of 5-LOX, 12-LOX, 15-LOX and COX pathways and further enzymatic pathways like various leukotriene-hydoxylases, leukotriene-, prostaglandin-, and thromboxane-synthases as well as various of their membrane based receptors are mainly significantly down-regulated in AD-patients vs. healthy volunteers. In addition, using HPLC MS-MS we determined up to 19 different metabolites originating from eicosapentaenoic acid (EPA), docosapentaenoic acid (DHA) and arachidonic acid (AA) ranging from hydroxylated-PUFA derivatives and further bioactive derivatives like thromboxanes, leukotrienes, prostaglandins and protectins originating from LOX and COX metabolism. In PBMCs from AD-patients LOX and COX pathways were down-regulated. We conclude from this study, that in PBMCs from AD-patients in comparison to healthy volunteers, a systemic down-regulation of LOX-and COX-responses occurs to generally reduce eicosanoid/docosanoid synthesis during the current allergic inflammatory status.

Original languageEnglish
Pages (from-to)35-42
Number of pages8
JournalProstaglandins and Other Lipid Mediators
Volume107
DOIs
Publication statusPublished - May 17 2013

    Fingerprint

Keywords

  • Atopic dermatitis
  • Cyclooxygenase pathway
  • Lipoxygenese pathway
  • PBMC

ASJC Scopus subject areas

  • Biochemistry
  • Physiology
  • Pharmacology
  • Cell Biology

Cite this