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The influence of anti-inflammatory lipoxin A4 on generation of cytokines by peripheral blood mononuclear cells of patients with psoriatic arthritis

100%
Łukasik Z., Kubiak M., Brzezinska O., Pomorska E., Lewandowska-Polak A., Kowalski M. L., Makowska J. S.
Alergia Astma Immunologia - przegląd kliniczny
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2021
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vol. 26
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issue 2-3
76-80
PL
Wprowadzenie: Patogeneza łuszczycowego zapalenie stawów (ŁZS), które występuje u ok. 40% pacjentów chorych na łuszczycę, jest nie do końca poznana i wyjaśniona. ŁZS obejmuje stawy osiowe (kręgosłup i stawy krzyżowo-biodrowe), stawy obwodowe, więzadła, ścięgna i przyczepy ścięgniste. Jedna z hipotez mówi, że powtarzające się mikrourazy oraz upośledzenie mechanizmów rezolucji procesu zapalnego, prowadzi do przewlekłego zapalenia, które obejmuje otaczające tkanki. Do mediatorów, prowadzących do ustąpienia stanu zapalnego w warunkach fizjologicznych należą lipoksyny pochodzące z kwasu arachidonowego. Cel pracy: Celem pracy było porównanie wpływu lipoksyny A4 na syntezę cytokin prozapalnych przez komórki jednojądrowe krwi obwodowej (PBMC) izolowane z krwi obwodowej pacjentów chorych na ŁZS i osób zdrowych. Metody: Do badania włączono 10 pacjentów chorych na łuszczycowe zapalenie stawów oraz 5 osób zdrowych. Komórki jednojądrowe krwi obwodowej izolowano techniką wirowania w gradiencie gęstości, a następnie inkubowano z lipopolisacharydem Escherichia coli O111:B4 z dodatkiem lub bez lipoksyny A4 przez 24 godziny. Poziomy IL-1β, IFN-α, IFN-γ, TNFα, MCP-1, IL-6, IL-8, IL-10, IL-17, IL-12, IL-18, IL-23 i IL -33 w supernatantach hodowli komórkowej oznaczono metodą cytometrii przepływowej. Wyniki: Inkubacja PBMC z LPS zwiększała produkcję wszystkich cytokin zarówno u pacjentów z łuszczycowym zapaleniem stawów i osób zdrowych. W PBMC osób zdrowych inkubacja komórek z lipoksyną A4 zmniejszała wytwarzanie cytokin prozapalnych. Jednak u pacjentów z łuszczycowym zapaleniem stawów dodanie lipoksyny A4 nie hamowało indukowanego przez LPS uwalniania cytokin prozapalnych. Wnioski: Przeciwzapalne działanie lipoksyny A4 jest odwrócone w PBMC u chorych na ŁZS, co potwierdza hipotezę o zaburzeniach rezolucji zapalenia w patogenezie ŁZS.
EN
Background: Up to 40% of patients with psoriasis suffer from psoriatic arthritis (PsA), an underrecognized inflammatory arthropathy of incompletely understood pathogenesis. PsA affects axial joints, surrounding ligaments, tendons and entheses. One hypothesis links repeated microinjuries with disorders of inflammation resolution mechanisms that lead to chronic inflammation, which spreads to surrounding tissues. An example of the mediators which lead to resolution of inflammation in physiological conditions are derivatives of arachidonic acid – lipoxins. Objectives: The aim of the study was to compare if the influence of lipoxin A4 on the synthesis of pro-inflammatory cytokines by peripheral blood mononuclear cells (PBMCs) isolated from peripheral blood of patients with PsA and healthy individuals. Methods: 10 patients with PsA and 5 matching healthy controls were enrolled in the study. PBMSc were isolated by gradient-density centrifugation technique and incubated with lipopolysaccharide with or without the addition of lipoxin A4 for 24 hours. The levels of IL-1β, IFN-α, IFN-γ, TNFα, MCP-1, IL-6, IL-8, IL-10, IL-17, IL-12, IL-18, IL-23 and IL-33 in cell culture supernatants were quantified by cytometric bead array system. Results: Incubation of PBMCs with LPS, increased production of all cytokines assessed either in patients with psoriatic arthritis or in healthy controls. In PBMCs from healthy controls incubation of cells with lipoxine A4 decrease production of proinflammatory cytokines. However, in patients with psoriatic arthritis addition of lipoxine A4 did not inhibited LPS – induced proinflammatory cytokines release. Conclusions: The anti-inflammatory effect of lipoxin A4 is reversed in PsA PBMCs, supporting the hypothesis of defective resolution of inflammation in the pathogenesis of PsA.
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Arachidonic acid-induced apoptosis in rat hepatoma AS-30D cells is mediated by reactive oxygen species

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Dymkowska D., Wojtczak L.
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issue 4
711-715
EN
Arachidonic acid at micromolar concentrations produced a drastic increase of the generation of reactive oxygen species (ROS) in rat hepatoma AS-30D cells cultivated in vitro along with an increase in the incidence of apoptotic cell death. Both processes were prevented by trolox, a water-soluble tocopherol derivative, and tempol, a known antioxidative agent. A synthetic hybrid of lipoic acid and trolox or preincubation with N-acetylcysteine were less effective. Preincubation of the cells with etomoxir, a known highly specific irreversible inhibitor of carnitine-palmitoyltransferase I, partly decreased the ROS formation induced by arachidonic acid but it did not affect the increase in apoptosis. Cumulatively, these results indicate that apoptosis induced in hepatoma cells by arachidonic acid is mediated by ROS. They also suggest that this effect is due to arachidonic acid as such and not to its mitochondrial oxidative metabolites.
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Amyloid beta enhances cytosolic phospholipase A2 level and arachidonic acid release via nitric oxide in APP-transfected PC12 cells

84%
Chalimoniuk M., Stolecka A., Cąkała M., Hauptmann S., Schulz K., Lipka U., Leuner K., Eckert A., Muller W. E., Strosznajder J. B.
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EN
Cytosolic phospholipase A2 (cPLA2) preferentially liberates arachidonic acid (AA), which is known to be elevated in Alzheimer's disease (AD). The aim of this study was to investigate the possible relationship between enhanced nitric oxide (NO) generation observed in AD and cPLA2 protein level, phosphorylation, and AA release in rat pheochromocytoma cell lines (PC12) differing in amyloid beta secretion. PC12 control cells, PC12 cells bearing the Swedish double mutation in amyloid beta precursor protein (APPsw), and PC12 cells transfected with human APP (APPwt) were used. The transfected APPwt and APPsw PC12 cells showed an about 2.8- and 4.8-fold increase of amyloid β (Aβ) secretion comparing to control PC12 cells. An increase of NO synthase activity, cGMP and free radical levels in APPsw and APPwt PC12 cells was observed. cPLA2 protein level was higher in APPsw and APPwt PC12 cells comparing to PC12 cells. Moreover, phosphorylated cPLA2 protein level and [3H]AA release were also higher in APP-transfected PC12 cells than in the control PC12 cells. An NO donor, sodium nitroprusside, stimulated [3H]AA release from prelabeled cells. The highest NO-induced AA release was observed in control PC12 cells, the effect in the other cell lines being statistically insignificant. Inhibition of cPLA2 by AACOCF3 significantly decreased the AA release. Inhibitors of nNOS and γ-secretase reduced AA release in APPsw and APPwt PC12 cells. The basal cytosolic [Ca2+]i and mitochondrial Ca2+ concentration was not changed in all investigated cell lines. Stimulation with thapsigargin increased the cytosolic and mitochondrial Ca2+ level, activated NOS and stimulated AA release in APP-transfected PC12 cells. These results indicate that Aβ peptides enhance the protein level and phosphorylation of cPLA2 and AA release by the NO signaling pathway.
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