Source: International Congress 2014 – New mechanisms in the pathogenesis of asthma and other lung diseases
Disease area: Airway diseases

Abstract

The aim of study is to analyze expression of negative regulator of transcription SOCS3 in peripheral blood of patients with allergic & non-allergic asthma (BA).Materials and methods. 20 healthy controls, 51 with allergic and 39 non-allergic BA patients were examined. Expression of SOCS3 protein was analyzed by Western blotting. Western blotting was performed through standard procedure. Antibodies against SOCS3 (Santa Cruz Biotechnology, UK) were used. Level of protein was analyzed according to b-actin using anti-actin antibodies (Sigma Aldrich, USA). Lymphocytes derived from patients were additionally analyzed after 1h incubation with and without IL-4 10 ng/ml.Results. We received differences in expression of SOCS3 with and without IL-4 (p=0,012 and p=0,033; Kruskal-Wallis crit.) in every group. We determined increase of SOCS3 expression in mononuclears of peripheral blood in allergic (p=0,022, crit. of Kolmogorov-Smirnov) and non-allergic BA (p=0,002, crit. of Kolmogorov-Smirnov) in comparison with control group. However, significant differences after action of IL-4 were estimated only in non-allergic BA group (p=0,007, crit. of Kolmogorov-Smirnov) compared with control. The effect of IL-4 resulted in increase of SOCS3 expression in all groups. We observed significant correlations between the level of SOCS3 expression and level of FEV1 in bronchodilation test (R=-0,44, p=0,001) and the dayly dose of corticosteroids in patients with allergic BA (R=0,4, p=0,004).Conclusion. The increase of SOCS3 can play important role as the marker of inflammation in asthma and may significantly correlate with main clinical characteristics (FEV1) of severity in allergic asthma.

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Citations should be made in the following way:
V. Mineev, L. Sorokina, M. Nyoma, V. Lim, V. Trofimov (Saint-Petersburg, Russian Federation). The expression of the negative regulator of gene transcription SOCS3 as the crucial marker in the asthma pathogenesis. Eur Respir J 2014; 44: Suppl. 58, 3864

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