RT Journal Article
SR Electronic
T1 The complex role of SOCS1 expression in peripheral blood mononuclears of patients with bronchial asthma
JF European Respiratory Journal
JO Eur Respir J
FD European Respiratory Society
SP P802
VO 40
IS Suppl 56
A1 Lada Sorokina
A1 Valeriy Mineev
A1 Valeria Lim
A1 Michael Nyoma
A1 Anna Eremeeva
A1 Yulia Malfygina
A1 Vasiliy Ivanov
A1 Vasiliy Trofimov
YR 2012
UL http://erj.ersjournals.com/content/40/Suppl_56/P802.abstract
AB The aim of the study is to analyze an expression of a negative regulator of cytokine signaling SOCS1 in peripheral blood of patients with allergic (ABA) and non-allergic bronchial asthma (NABA).Materials and methods. 14 healthy controls, 40 patients with allergic (atopic) and 33 with non-allergic BA were examined. The expression of SOCS1 mRNA was analyzed by RT-PCR. Primers of SOCS1 have been developed on the basis of known sequences (GenBank). Expression level of mRNA SOCS1 was estimated relatively to level of β-actin mRNA. Preparation of cell lysates, and the Western blotting were performed through the standard procedure. Anti-SOCS1 antibodies (Santa Cruz Biotechnology, UK) were used. The level of protein was analyzed relatively to β-actin using anti-actin antibodies (Sigma Aldrich, USA).Results.We determined the decrease (in 5,4 times) of SOCS1 expression in peripheral blood mononuclears in patients with ABA in comparison with healthy persons (p=0,036) and NABA patients (in 5,3 times) (p=0,024) (U-criterion). NABA patients had no significant difference in comparison with healthy persons. SOCS1 mRNA expression level in peripheral blood mononuclears in ABA patients was significantly lower than in the healthy persons (in 1,4 times) (p=0,048; crit. Tukey) and NABA patients (in 1,3 times) (p=0,041; crit. Tukey).Conclusion. SOCS1 may play an important role in pathogenesis of bronchial asthma. Decrease of SOCS1, and SOCS1 mRNA expression in patients with ABA may be sign of defect in negative regulation system of cytokine signaling. It may be caused by genetic based impairment of SOCS1 expression regulation either on transcription or further levels (translation, protein levels).