EXPRESSION FEATURES OF TOLL-LIKE RECEPTOR 2 AND TOLL-LIKE RECEPTOR 4 IN CHILDREN WITH ASTHMA
Currently actively discussed the role of innate immunity receptors, in particular TLRs in the immunopathogenesis of bronchial asthma (BA). The aim of our work was to study the expression of ТLR2 and TLR4 on the nasal mucosal cells and peripheral blood leukocytes of patients with BA of different seve...
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Veröffentlicht in: | Medit͡s︡inskai͡a︡ immunologii͡a 2017-01, Vol.19 (4), p.431 |
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Zusammenfassung: | Currently actively discussed the role of innate immunity receptors, in particular TLRs in the immunopathogenesis of bronchial asthma (BA). The aim of our work was to study the expression of ТLR2 and TLR4 on the nasal mucosal cells and peripheral blood leukocytes of patients with BA of different severity. The study included 40 children with asthma (3-12 years) and 10 healthy children. Methods: real-time PCR, flow cytometry and multiplex immunofluorescence analysis evaluated the levels of pro and anti-inflammatory cytokines (IL-1β, IL-1ra, IL-6, IL-8, IL-10, TNFα) in nasal swabs. The result of the study hyperactivation of the factors of innate immunity at the level of the mucosal of the nasal cavity in patients with asthma, manifested by increased gene expression of TLR2, TLR4, and production of proinflammatory as well as anti-inflammatory cytokines. Correlation between cytokine levels and the severity of asthma. In the peripheral blood identified a significant increase in the expression of TLR2 and TLR4 on circulating CD14+ monocytes in children with BA. Thus, the increase of gene expression of TLRs mucosa of the nasal cavity, increase surface expression of TLR2 and TLR4 on circulating monocytes of patients with bronchial asthma compared to healthy children. The revealed changes indicate the involvement of the system of TLRs in the immunopathogenesis of bronchial asthma. In the future, TLRs can be used as markers to predict the course of ad and possible therapeutic targets. |
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ISSN: | 1563-0625 2313-741X |
DOI: | 10.15789/1563-0625-2017-4-431-440 |