Harsha H Kariyawasam1, Giuseppina Rotiroti. 1. Allergy and Medical Rhinology Section, Royal National Throat Nose Ear Hospital, UCLH NHS Foundation Trust, University College London, London, UK. harsha.kariyawasam@uclh.nhs.uk
Abstract
PURPOSE OF REVIEW: Allergic rhinitis, chronic rhinosinusitis (CRS) and asthma have a high worldwide prevalence and confer a significant socioeconomic burden. This article reviews the recent advances in allergic rhinitis, CRS and asthma with view to understanding the upper and lower airway as one system. RECENT FINDINGS: Allergic rhinitis, CRS and asthma demonstrate strong epidemiological coassociation, and early life risk factors for upper airway disease are now apparent. The absence of demonstrable peripheral IgE does not strictly classify airway disease as nonallergic. Excess mucosal inflammation with immune dysregulation is a common feature to all. An important role for innate immunity is now apparent and offers prospects of novel therapeutic approaches in the future. A role for bacterial superantigens is also emerging in all three diseases. Genetic studies highlight common associations between allergic rhinitis, CRS and asthma. SUMMARY: Whether such overlapping pathological findings reflect a manifestation of the same disease but in relation to the different airway locations in individuals with genetic predisposition remains unknown, although likely. This continues under investigation and debate. The current research priorities are to understand what key events predispose to both upper and lower airway disease together and the critical immunological factors that establish and sustain airway inflammation.
PURPOSE OF REVIEW: Allergic rhinitis, chronic rhinosinusitis (CRS) and asthma have a high worldwide prevalence and confer a significant socioeconomic burden. This article reviews the recent advances in allergic rhinitis, CRS and asthma with view to understanding the upper and lower airway as one system. RECENT FINDINGS:Allergic rhinitis, CRS and asthma demonstrate strong epidemiological coassociation, and early life risk factors for upper airway disease are now apparent. The absence of demonstrable peripheral IgE does not strictly classify airway disease as nonallergic. Excess mucosal inflammation with immune dysregulation is a common feature to all. An important role for innate immunity is now apparent and offers prospects of novel therapeutic approaches in the future. A role for bacterial superantigens is also emerging in all three diseases. Genetic studies highlight common associations between allergic rhinitis, CRS and asthma. SUMMARY: Whether such overlapping pathological findings reflect a manifestation of the same disease but in relation to the different airway locations in individuals with genetic predisposition remains unknown, although likely. This continues under investigation and debate. The current research priorities are to understand what key events predispose to both upper and lower airway disease together and the critical immunological factors that establish and sustain airway inflammation.
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