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1
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Lung protection in cardio-pulmonary bypass

100%
Salameh A., Greimann W., Vollroth M., Dhein S., Bahramsoltani M., Dahnert I.
Journal of Physiology and Pharmacology
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2017
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tom 68
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nr 1
2

PDE4 inhibitors have no effect on eotaxin expression in human primary bronchial epithelial cells

100%
Paplinska-Goryca M., Chazan R., Grubek-Jaworska H.
Acta Biochimica Polonica
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2012
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tom 59
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nr 3
 The bronchial epithelium is a very important factor during the inflammatory response, it produces many key regulators involved in the pathophysiology of asthma and COPD. Local influx of eosinophils, basophils, Th2 lymphocytes and macrophages is the source of many cytotoxic proteins, cytokines and other mediators of inflammation. These cells are attracted by eotaxins (eotaxin-1/CCL11, eotaxin-2/CCL24, eotaxin-3/CCL26). Inhibitors of phosphodiesterase 4 (PDE4) are new anti-inflammatory drugs which cause cAMP accumulation in the cell and inhibit numerous stages of allergic inflammation. The aim of our study was to evaluate the influence of PDE4 inhibitors: rolipram and RO-20-1724 on the expression of eotaxins in human primary bronchial epithelial cells. Cells were preincubated with PDE4 inhibitors for 1 hour and then stimulated with IL-4 or IL-13 alone or in combination with TNF-α. After 48 hours, eotaxin protein level was measured by ELISA and mRNA level by real time PCR. These cells produce CCL24 and CCL26. PDE4 inhibitors increased CCL24 and CCL26 mRNA level irrespectively of the used stimulators. Rolipram and RO-20-1724 had no effect on eotaxin protein production in our experimental conditions. Thus PDE4 inhibitors have no effect on eotaxin protein expression in human primary bronchial epithelial cells. In vitro experiments should be performed using a primary cell model rather than immortalized lines.
3
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Effect of aspirin on cysteinyl leukotrienes production by eosinophils co-cultured with epithelial cells

84%
Jawien J., Olszanecki R., Lorkowska B., Korbut R.
Journal of Physiology and Pharmacology
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2004
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tom 55
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nr 4
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 (PGE2) 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 PGE2 was decreased by aspirin (n=32). BEAS-2B cells barely formed Cys-LTs; addition of ASA increased this production, while production of PGE2 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.
4
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Relationship between airway wall thickness assessed by high-resolution computed tomography and lung function in patients with asthma and chronic obstructive pulmonary disease

67%
Kosciuch J., Krenke R., Gorska K., Zukowska M., Maskey-Warzechowska M., Chazan R.
Journal of Physiology and Pharmacology. Supplement
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2009
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tom 60
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nr 5
5
Content available remote

Effects of cigarette smoke on the lung and systemic immunity

67%
Domagala-Kulawik J.
Journal of Physiology and Pharmacology. Supplement
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2008
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tom 59
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nr 6
19-34
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