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1

Onset and persistence of the allergic inflammation: a molecular explanation?

100%
Spinozzi F.
Archivum Immunologiae et Therapiae Experimentalis
|
1998
|
tom 46
|
nr 5
2
Content available remote

Cough reflex sensitivity is increased in the guinea pig model of allergic rhinitis

84%
Brozmanova M., Plevkova J., Tatar M., Kollarik M.
Journal of Physiology and Pharmacology. Supplement
|
2008
|
tom 59
|
nr 6
153-161
3

Hypoxia-inducible factor 1 as one of the 'signaling drivers' of toll-like receptor-dependent and allergic inflammation

84%
Sumbayev V. V., Nicholas S. A.
Archivum Immunologiae et Therapiae Experimentalis
|
2010
|
tom 58
|
nr 4
287-294
4

Innate lymphoid cells in type 2 immune responses

84%
Mirchandani A. S., Salmond R. J.
Archivum Immunologiae et Therapiae Experimentalis
|
2015
|
tom 63
|
nr 3
5

Positive and negative regulatory mechanisms in high-affinity IgE receptor-mediated mast cell activation

84%
Roth K., Chen W.-M., Lin T.-J.
Archivum Immunologiae et Therapiae Experimentalis
|
2008
|
tom 56
|
nr 6
385-399
6

The role of PTEN in allergic inflammation

84%
Lee Y. C.
Archivum Immunologiae et Therapiae Experimentalis
|
2004
|
tom 52
|
nr 4
7
Content available remote

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
|
2004
|
tom 55
|
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.
8

Heparin modulates migration of human peripheral blood mononuclear cells and neutrophils

84%
Zak-Nejmark T., Krasnowska M., Jankowska R., Jutel M.
Archivum Immunologiae et Therapiae Experimentalis
|
1999
|
tom 47
|
nr 4
9
Content available remote

Effect of phosphodiesterase 4 (PDE4) inhibitors on eotaxin expression in human bronchial epithelial cells

67%
Paplinska M., Chazan R., Grubek-Jaworska H.
Journal of Physiology and Pharmacology
|
2011
|
tom 62
|
nr 3
The increasing number of eosinophils into bronchoaelvolar space is observed during noninfectious inflammatory lung diseases. Eotaxins (eotaxin-1/CCL11, eotaxin-2/CCL24, eotaxin-3/CCL26) are the strongest chemotactic agents for eosinophils. Inhibitors of phosphodiesterase 4 (PDE4), the enzyme decomposing cAMP, are anti-inflammatory agents which act through cAMP elevation and inhibit numerous steps of allergic inflammation. The effect of PDE4 inhibitors on eotaxin expression is not known in details. The aim of our study was to evaluate the influence of PDE4 inhibitors: rolipram and RO-20-1724 on expression of eotaxins in bronchial epithelial cell line BEAS-2B. Cells were preincubated with PDE4 inhibitors or dexamethasone for 1 hour and then stimulated with IL-4 or IL-13 alone or in combination with TNF-. After 48 hours eotaxin protein level was measured by ELISA and mRNA level by real time PCR. Results: PDE4 inhibitors decreased CCL11 and CCL26 expression only in cultures co-stimulated with TNF-. In cultures stimulated with IL-4 and TNF- rolipram and RO-20-1724 diminished CCL11 mRNA expression by 34 and 37%, respectively, and CCL26 by 43 and 47%. In cultures stimulated with IL-13 and TNF- rolipram and RO-20-1724 decreased expression of both eotaxins by about 50%. These results were confirmed at the protein level. The effect of PDE4 inhibitors on eotaxin expression in BEAS-2B cells, in our experimental conditions, depends on TNF- contribution.
10

Chemokine RANTES in atopic dermatitis

67%
Gluck J., Rogala B.
Archivum Immunologiae et Therapiae Experimentalis
|
1999
|
tom 47
|
nr 6
11

The role of thymic stromal lymphopoietin in allergic inflammation and chronic obstructive pulmonary disease

59%
Fang C., Siew L. Q. C., Corrigan C. J., Ying S.
Archivum Immunologiae et Therapiae Experimentalis
|
2010
|
tom 58
|
nr 2
81-90
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