Expression of Micro RNA-155 Is Induced By Dust Mite Extract in CD4+ T-Cells of Dust Mite Allergic Subjects and Is Inhibited By Glucocorticoids
Sunday, March 6, 2016: 2:45 PM
Room 406AB (Convention Center)
Elizabeth M. Balraj, ,

MicroRNAs (miRNAs) are emerging as important regulators of allergic inflammation and potential therapeutic targets.  We hypothesized that allergic stimuli alter miRNA expression in T-cells and that glucocorticoids modulate this process.


After IRB approval, blood was collected from dust mite (DM) allergic subjects (n=19) and non-allergic controls (n=9).  Peripheral blood mononuclear cells were incubated with dust mite extract (DME), diluent control, or DME + dexamethasone (0.1 µM).  CD4+ T-cells were collected by magnetic bead column, and RNA was isolated by guanidinium/phenol-chloroform extraction.  MicroRNA expression was screened by Nanostring microarray and data was validated by quantitative real time PCR (qPCR). 


Nanostring profiling was used to screen T-cell miRNA expression in n=6 dust mite allergic and n=6 non-allergic subjects.  There were no differences in the miRNAs detected in T-cells when comparing allergic with non-allergic subjects in the absence of DM extract stimulation. MiR-155 was significantly increased in the DM-allergic T-cells after DME stimulation (2.1 ± 0.4 fold change), but no significant changes were seen in non-allergic cells (1.3 ± 0.2 fold change). Using a larger sample size (n=19 dust mite allergic, n=9 non-allergic), changes in miR-155 after DME stimulation were confirmed by qPCR (4.3 ± 1.98 fold change in allergics, 0.9 ± .19, non-allergics).  Dexamethasone inhibited the DME-induced miR-155 change in asthmatics.


MiR-155 is differentially expressed in allergic T-cells exposed to DM extract compared to non-allergic cells, and is inhibited by glucocorticoids.  MiR-155 may play a role in mediating allergic inflammation in T-cells and could be an anti-inflammatory target of steroids.