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B Lorkowska

Publications and source records attributed to B Lorkowska.

3 recordsLinked to original sources

Hypercholesterolemia does not alter endothelial function in spontaneously hypertensive rats.

In humans, hypercholesterolemia and hypertension are associated with endothelial dysfunction. Here, we assess whether hypercholesterolemia induces endothelial dysfunction in rats with pre-existing hypertension. Spontaneously hypertensive rats (SHR) and normotensive controls (WKY) were fed with a high-cholesterol diet for 12 weeks, and endothelial function was assessed in isolated thoracic aortic rings. In SHR and WKY rats, the hypercholesterolemic diet resulted in the elevation of total cholesterol and low-density lipoprotein levels by approximately 2.5- and 4.5-fold, respectively. However, in aorta, the basal nitric oxide (NO) production--as assessed by the magnitude of L-NG-nitroarginine methyl ester-induced vasoconstriction as well as the NO-dependent relaxation induced by acetylcholine or histamine--were not diminished either in SHR or in WKY rats fed with the hypercholesterolemic diet. Interestingly, prostacyclin (PGI2) production in aortic rings from SHR rats was higher than in the aorta from WKY rats. However, the hypercholesterolemic diet had no further effects on PGI2 production in the aorta either of SHR or WKY rats. The monocyte chemoattractant protein 1 level in plasma was slightly elevated in SHR and WKY rats fed with the hypercholesterolemic diet compared with their normocholesterolemic counterparts. In summary, even in the presence of pre-existing hypertension, hypercholesterolemia fails to modify NO-dependent and PGI2-dependent endothelial function in SHR rats; it also does not induce a robust inflammatory response. Both are prerequisites for the development of atherosclerosis.

Animals↗

Effect of aspirin on cysteinyl leukotrienes production by eosinophils co-cultured with epithelial cells.

Eosinophils have long been considered to play solely crucial role in the pathogenesis of aspirin-induced asthma, however increasing evidence suggest that the bronchial epithelium is also involved in the initiation and maintenance of allergic inflammation. Epithelial cells and eosinophils retained within airways interact reciprocally to mount and sustain inflammatory response. Recently, we have shown that eosinophil-epithelial cell interactions are capable of amplifying the production of cysteinyl leukotrienes (Cys-LTs). The aim of this study was to investigate if there is any influence of aspirin (ASA) on Cys-LTs and prostaglandin E2 (PGE(2)) production in the model of co-cultured human epithelial cells (line BEAS-2B) and human eosinophils. Synthesis of Cys-LTs in eosinophils was increased after incubation with ASA. At the same time the production of PGE(2) was decreased by aspirin (n=32). BEAS-2B cells barely formed Cys-LTs; addition of ASA increased this production, while production of PGE(2) was inhibited by aspirin (n=32). Synthesis of Cys-LTs by eosinophils co-incubated with BEAS-2B was nearly 7-fold higher than that of activated eosinophils alone (1631.5 pg/ml +/- 154 vs. 258 pg/ml +/- 31; p<0.05; n=32). Surprisingly, in the eosinophil-epithelial cell co-culture, aspirin inhibited both augmentation of Cys-LTs synthesis (from 1631.5 pg/ml +/- 154 to 1458 pg/ml +/- 137; p<0.05; n=32) and the production of PGE2 (from 2640 pg/ml +/- 231 to 319 pg/ml +/- 27; p<0.05; n=32). In summary, we have demonstrated that interactions between non-atopic eosinophils and epithelial cells result in augmentation of Cys-LTs production, and this augmentation could be inhibited by aspirin.

Aspirin↗

Eosinophil-epithelial cell interaction augments cysteinyl leukotrienes synthesis.

Eosinophils accumulation in the airways and sustained eosinophil-derived cysteinyl leukotrienes production represent key elements of the inflammatory response seen in asthma. However, it is not known whether activated epithelial cells influence cysteinyl leukotrienes production by eosinophils from healthy valunteers. The aim of the present study was therefore to analyse the effects of interactions between non-atopic eosinophils and epithelial cells on cysteinyl leukotrienes production in vitro. We measured cysteinyl leukotrienes released by phorbol 12-myristate 13-acetate (PMA) -activated human eosinophils or epithelial cells (human bronchial epithelial cell line -BEAS-2B) cultured alone or together. While activated BEAS-2B cells barely formed leukotrienes (1.39 pg/ml +/- 0.2) (n=32), activated eosinophils produced considerable amount of them (62.25 pg/ml +/- 10.29) (n=32). Interestingly, when activated eosinophils and epithelial cells were co-incubated, production of cysteinyl leukotrienes increased substantially (571.1 pg/ml +/- 80.9) (n=32). Thus, eosinophil-epithelial cell interactions, when occur, are associated with increased biosythesis of cysteinyl leukotrienes.

Bronchi↗