TDI (Toluene 2, 4-diisocyanate) is one of the leading causes of chemical-induced occupational asthma. MicroRNAs are small, noncoding RNAs that exhibit profound functional significance through the inhibition of gene expression of mRNA targets. Recently, the robust regulatory potential of miRNAs has become apparent, including their functional role in the regulation of allergic disease. Our laboratory has previously showed that miRNA 210 expression is significantly augmented in the draining lymph nodes of mice dermally dosed with TDI at various time points post exposure, however, the specific role of miRNA 210 in chemical sensitization is unknown. In this work, to elucidate the functional role of miRNA 210 during TDI sensitization, BALB/c mice were dermally exposed to TDI (4% v/v) or vehicle and endpoints were evaluated via RT-PCR, magnetic cell separation, and flow cytometry. Draining lymph node CD4+ cells showed significantly increased miRNA 210 expression following a single exposure to TDI. Confirmed (foxp3) and predicted (runx1t1, runx3, smad4, and stat6) miRNA 210 transcription factor target expression was evaluated and augmentations in foxp3 cellular protein expression and decreases in runx1 and foxp3 mRNA were observed. This data indicates that miRNA 210 has a functional role in TDI sensitization which may be related to regulatory T cell differentiation and function.
Allergies; Allergic-disorders; Genes; Toluenes; Isocyanates; Ribonucleic-acids; Laboratory-animals; Laboratory-testing; Exposure-assessment; Exposure-levels; Exposure-methods; Lymph-nodes; Cytochemistry; Sensitization; Cell-division; Cellular-reactions; Cell-differentiation; Cellular-function; Chemical-hypersensitivity; Bronchial-asthma