Abstract
Chronic upper airway inflammation is amongst the most prevalent chronic disease entities in the Western world with prevalence around 30% (rhinitis) and 11% (rhinosinusitis). Chronic rhinitis and rhinosinusitis may severely impair the quality of life, leading to a significant socio-economic burden. It becomes more and more clear that the respiratory mucosa which forms a physiological as well as chemical barrier for inhaled particles, plays a key role in maintaining homeostasis and driving disease. In a healthy state, the mucosal immune system provides protection against pathogens as well as maintains a tolerance toward non-harmful commensal microbes and benign environmental substances such as allergens. One of the most important players of the mucosal immune system is immunoglobulin (Ig) A, which is well-studied in gut research where it has emerged as a key factor in creating tolerance to potential food allergens and maintaining a healthy microbiome. Although, it is very likely that IgA plays a similar role at the level of the respiratory epithelium, very little research has been performed on the role of this protein in the airways, especially in chronic upper airway diseases. This review summarizes what is known about IgA in upper airway homeostasis, as well as in rhinitis and rhinosinusitis, including current and possible new treatments that may interfere with the IgA system. By doing so, we identify unmet needs in exploring the different roles of IgA in the upper airways required to find new biomarkers or therapeutic options for treating chronic rhinitis and rhinosinusitis.
Highlights
Chronic inflammatory upper airway diseases are among the most prevalent chronic disease entities impacting the life of about 25% of the population in the Western World [1, 2]
At the level of the intestinal mucosa, it is known that immunoglobulin A (IgA) binds to the surface of certain members of the intestinal microbiota and for the majority of these microbes, this does not lead to their clearance from the intestinal system [57]
Two studies reported on an overexpression of BAFF, an important inducer of local IgA class switching, in CRS with NP (CRSwNP) patients [112, 115]. These findings indicate an increase in the local IgA production by type 2 inflamed polyp tissue and most of the plasma cells detected in NP tissue are of the IgA producing type [118]
Summary
Chronic inflammatory upper airway diseases are among the most prevalent chronic disease entities impacting the life of about 25% of the population in the Western World [1, 2]. In the absence of additional signals, the recognition of ICs by FcαRI facilitates the uptake of antigens which leads to only a partial activation of DCs and does not trigger any proinflammatory responses [41] This function is key in the induction of the development of mucosal tolerance to, e.g., certain inhaled allergens where S-IgA seems to play a role (see below), still very little is known about its mechanisms. IgA levels in nasal lavages were shown to correlate with nasal symptoms [96] This view of the IgA response as a pathogenic mechanism in AR acting along with IgE, is contested by several observations: first, SIgAD or delayed serum IgA production in childhood is a well-known risk factor for atopy [97, 98] and patients with sIgAD suffer more frequently from AR compared to the general population [71, 72]. No significant differences in Frontiers in Allergy | www.frontiersin.org
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