Immunological and microRNA Features of Allergic Rhinitis in the Context of United Airway Disease

Abstract

Inflammation of the upper respiratory tract in patients with allergic rhinitis (AR) may contribute to lower respiratory airways’ inflammation. T-helper 17 (Th17) cells and related cytokines are also involved in the immunological mechanism of AR along with the classical Th2 cells. It is hypothesized that upon Th2 pressure, the inflammatory response in the lungs may lead to Th17-induced neutrophilic inflammation. However, the findings for interleukin-17 (IL-17) are bidirectional. Furthermore, the role of Th17 cells and their counterpart—T regulatory cells—remains unclear in AR patients. It was also shown that a regulator of inflammation might be the individual circulating specific non-coding microRNAs (miRNAs), which were distinctively expressed in AR and bronchial asthma (BA) patients. However, although several circulating miRNAs have been related to upper and lower respiratory tract diseases, their function and clinical value are far from being clarified. Still, they can serve as noninvasive biomarkers for diagnosing, characterizing, and providing therapeutic targets for anti-inflammatory treatment along with the confirmed contributors to the pathogenesis—Th17 cells and related cytokines. The narrow pathogenetic relationship between the nose and the bronchi, e.g., upper and lower respiratory tracts, confirms the concept of unified airway diseases. Thus, there is no doubt that AR and BA should be diagnosed, managed, and treated in an integrated manner.