MicroRNA: endotyping united airways?

translation [3] . Given their very short complementarity to the target mRNA (6–8 nucleotides), a single miR can target hundreds of genes, and individual genes might be targeted by multiple mRNAs, adding complexity to the regulatory network between miRs and target genes [4] . MiRs are phylogenetically well conserved [5] , which implies that they play an important role in biological processes. In fact, they are thought to regulate more than 30% of all protein-coding genes [6] and have been found to be involved in the regulation of development [7] , proliferation [8] , differentiation [9] , apoptosis [10] and immune response [11] . The use of miR microarrays makes it possible to perform profiling studies that evaluate the differences between healthy and pathological tissues, treated and untreated samples and undifferentiated and differentiated cells [12] . Moreover, this systematic screening approach provides us with a starting point for the identification of new miR functions. Recent studies have identified miR profiles in multiple allergic inflammatory diseases, including asthma [13–16] , eosinophilic esophagitis [17] and atopic dermatitis [18] . Although the evaluation of miR expression and function in AR patients has received little attention, a growing number of publications have Allergic rhinitis (AR) is a significant health problem because of its high prevalence (10–50% of the population) and impact on patients’ symptoms and quality of life [1] . To fully understand this impact, its relation to other upper and lower respiratory diseases, particularly asthma, should be taken into account, since up to 80% of the asthmatic patients present with concomitant AR [2] . Both diseases involve IgE-mediated mechanisms and can be triggered by similar allergens, including mold, animal dander and house-dust mites. Sustained airway inflammation associated with marked changes in gene and protein expression under fine-tuned regulation is a hallmark of AR. For this reason, a better understanding of the mechanisms involved in inflammatory gene expression regulation in AR, whether associated with asthma or not, is critical for the development of new therapy approaches. A group of novel regulators of gene expression, purported to be involved in the modulation of the inflammatory process of diseases such as AR and asthma, are the socalled microRNAs (miRs). MiRs are short, single-stranded, noncoding RNAs of 20–23 nucleotides that downregulate gene expression by binding to the 3 ′ -untranslated region of their target mRNAs, which induce their degradation or impair their Published online: May 10, 2014