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Published on: April 16, 2019
Budesonide increases TLR4 and TLR2 expression in Treg lymphocytes of allergic asthmatics
Elisabetta Pace1, Caterina Di Sano1, Maria Ferraro1
1Istituto di Biomedicina e Immunologia Molecolare, Unità di Immunopatologia e Farmacologia Clinica e Sperimentale dell'Apparato Respiratorio, Consiglio Nazionale delle Ricerche, Palermo, Italy.
Background:
Reduced innate immunity responses as well as reduced T regulatory activities characterise bronchial asthma.
Objectives:
In this study the effect of budesonide on the expression of TLR4 and TLR2 in T regulatory lymphocyte sub-population was assessed.
Methods:
TLR4 and TLR2 expression in total peripheral blood mononuclear cells (PBMC), in CD4+/CD25+ and in CD4+/CD25- was evaluated, by flow cytometric analysis, in mild intermittent asthmatics (n = 14) and in controls (n = 11). The in vitro effects of budesonide in modulating: TLR4 and TLR2 expression in controls and in asthmatics; IL-10 expression and cytokine release (IL-6 and TNF-α selected by a multiplex assay) in asthmatics were also explored.
Results:
TLR4 and TLR2 were reduced in total PBMC from asthmatics in comparison to PBMC from controls. CD4+CD25+ cells expressed at higher extent TLR2 and TLR4 in comparison to CD4+CD25- cells. Budesonide was able to increase the expression of TLR4, TLR2 and IL-10 in CD4+/CD25 highly+ cells from asthmatics. TLR4 ligand, LPS induced Foxp3 expression. Budesonide was also able to reduce the release of IL-6 and TNF-α by PBMC of asthmatics.
Conclusions:
Budesonide potentiates the activity of Treg by increasing TLR4, TLR2 and IL-10 expression. This event is associated to the decreased release of IL-6 and TNF-α in PBMC treated with budesonide. These findings shed light on new mechanisms by which corticosteroids, drugs widely used for the clinical management of bronchial asthma, control T lymphocyte activation.
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