Abstract
Asthma is a chronic respiratory disease affecting people of all ages, especially children, worldwide. Origins of asthma are suggested to be placed in early life with heterogeneous clinical presentation, severity and pathophysiology. Exacerbations of asthma disease can be triggered by many factors, including viral respiratory tract infections. Rhinovirus (RV) induced respiratory infections are the predominant cause of the common cold and also play a crucial role in asthma development and exacerbations. Rhinovirus mainly replicates in epithelial cells lining the upper and lower respiratory tract. Type III interferons, also known as interferon-lambda (IFNλ), are potent immune mediators of resolution of infectious diseases but they are known to be involved in autoimmune diseases as well. The protective role of type III IFNs in antiviral, antibacterial, antifungal and antiprotozoal functions is of major importance for our innate immune system. The IFNλ receptor (IFNλR) is expressed in selected types of cells like epithelial cells, thus orchestrating a specific immune response at the site of viruses and bacteria entry into the body. In asthma, IFNλ restricts the development of TH2 cells, which are induced in the airways of asthmatic patients. Several studies described type III IFNs as the predominant type of interferon increased after infection caused by respiratory viruses. It efficiently reduces viral replication, viral spread into the lungs and viral transmission from infected to naive individuals. Several reports showed that bronchial epithelial cells from asthmatic subjects have a deficient response of type III interferon after RV infection ex vivo. Toll like Receptors (TLRs) recognize pathogen-associated molecular patterns (PAMPs) expressed on infectious agents, and induce the development of antiviral and antibacterial immunity. We recently discovered that activation of TLR7/8 resulted in enhanced IFNλ receptor mRNA expression in PBMCs of healthy and asthmatic children, opening new therapeutic frontiers for rhinovirus-induced asthma. This article reviews the recent advances of the literature on the regulated expression of type III Interferons and their receptor in association with rhinovirus infection in asthmatic subjects.
Highlights
ASTHMA AND ITS PATHOGENESISAsthma is a chronic respiratory disease affecting the life of millions of people worldwide
We recently discovered that activation of toll-like receptor 7 and 8 (TLR7/8) resulted in enhanced IFNl receptor mRNA expression in peripheral blood mononuclear cells (PBMC) of healthy and asthmatic children, opening new therapeutic frontiers for rhinovirus-induced asthma
We focus on the type III interferon family known as interferon-lambda 1-4
Summary
Asthma is a chronic respiratory disease affecting the life of millions of people worldwide. A large cohort study found an interaction between single nucleotide polymorphisms (SNPs) in the 17q21 locus, rhinovirus induced wheezing illness in childhood and asthma development [12] Despite these findings, it is still controversial whether RV infections are the cause or a result of susceptibility to allergens and pathogens of asthmatic subjects. We will further discuss the role of RV infections as common triggers of asthmatic exacerbations and how type III IFNs affect them [18]. In this narrative review, we will emphasize on the regulation and variability in the expression of interferon-lambda family members and the signaling via its receptor interferon-lambda receptor (IFNlR) [19]
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