@misc{Biedroń_Rafał_The_2005,
 author={Biedroń, Rafał},
 address={Kraków},
 howpublished={online},
 year={2005},
 school={Uniwersytet Jagielloński – Collegium Medicum},
 language={pol},
 abstract={The purpose of this study was to examine the mechanism of action of selected endo- and exogenous inflammatory eicosanoids: prostaglandin E2 (PGE2) and leukotrienes (LTs): leukotriene B4 (LTB4) and cysteinyl leukotrienes (cysLTs) in murine bone marrow-derived dendritic cells (DC). It was shown that opsonized zymosan (OZ) stimulated DC to release PGE2 as well as LTs. In contrast, lipopolysaccharide (LPS) treated DC produced only PGE2 by cyclooxygenase-2 activity, whereas 5-lipoxygenase catalyzed LTs synthesis. In our in vitro model PGE2 and LTs differentially modified cytokine release in activated DC. Briefly, exogenous PGE2, but not endogenous ones, inhibited the release of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and IL-12 p40 and enhanced the release of IL-10 from DC via EP2/EP4, DP and IP but not EP1, EP3 or FP prostanoid receptors. In contrast to LPS stimulated DC, OZ stimulated ones, released much more TNF-α, IL-6 and IL-10 and less IL-12 p40 and large amounts of LTs. Exogenous LTB4 and LTD4 increased IL-10 and down-regulated IL-12 p40 release from LPS stimulated DC, but LTD4 seemed to be a less potent regulator than LTB4. Blockade of endogenous LTs and LTB4 receptor (BLT1), but not CysLT1 receptor resulted in slightly lower IL-10 and higher IL-12 p40 production in OZ stimulated DC, but not LPS stimulated ones. In conclusion, endo- and exogenous LTs can affect},
 abstract={cytokine release in stimulated DC. In particular, LTB4 (through the action at BLT1) seems to be partially responsible for the higher IL-10 and lower IL-12 p40 release from OZ-stimulated DC as compared to LPS-stimulated ones.},
 title={The role of eicosanoids in the regulation of bone marrow-derived dendritic cells function},
 type={Praca doktorska},
 keywords={murine bone marrow-derived dendritic cells, eicosanoids, leukotrienes, cytokines, prostaglandins},
}