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Mutual Interaction of Prostate Carcinoma And Benign Prostate Hyperplasia Cells With Human Lymphocyte Mononuclear Cells – Modulation of Parameters of Innate Immunity by PPAR‐gamma ligands
Author(s) -
Koenig Wolfgang,
Allhoff Ernst Peter,
Ghebremedhin Beniam,
Koenig Brigitte,
Tammer Ina,
Koenig Jens Ekkehard
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.570.14
Subject(s) - lymphocyte , tlr2 , peripheral blood mononuclear cell , innate immune system , receptor , cancer research , endocrinology , medicine , biology , chemistry , microbiology and biotechnology , immunology , in vitro , biochemistry
We studied the mutual interaction of human lymphocyte mononuclear cells on co‐incubation with prostate carcinoma (PCA) and BPH cells in the presence of 15d‐PGJ2 and glitazones (troglitazone, ciglitazone). The cells were stimulated with growth factors (VEGF, EGF, HGF, IGF, FGF) at various concentrations (1‐100 ng). PPAR‐gamma ligands at various concentrations were either added prior to or after co‐incubation with PCA and BPH cells for 24 hours; the release of mediators (IL‐6, IL‐8, TNF‐alpha, VEGF, TGF‐beta, PGE 2 ) was studied by Elisa; RT‐PCR and Taqman analysis were applied for the analysis of parameters of innate immunity, e. g. p22‐, 47‐, 67‐, gp91‐phox, cysteinylleukotriene receptors 1, 2, protease activated receptors (PAR1‐4), toll‐like receptors (TLR2, 4, 9), COX2, CD14, TRAF6, MD2, MYD88, CXCR2. Our results show: 1) Human lymphocyte mononuclear cells modulate various parameters of innate immunity on carcinoma as well as BPH cells after co‐incubation. 2) PPAR‐gamma‐ligands interact differently when given prior or after co‐incubation of tumor cells with human lymphocyte mononuclear cells. 3) Differences in pro‐ and antiinflammatory responses depend on the individual cell line as well as the stimulus via differences in cellular signal transduction. The results suggest a potential use of PPAR‐gamma‐ligands to dampen inflammation and potentially tumor development.

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