Abstract
Great strides have been made in the last five years in understanding the pathology of chronic rhinosinusitis (CRS). CRS is now accepted to be the end-stage manifestation of inflammation resultant from various pathogenetic mechanisms. This has resulted in increasing recognition of distinct CRS endotypes. Such endotypes encompass a cluster of patients with similar pathogenic mechanisms that may have common therapeutic targets and responsiveness to interventions. The elucidation of mechanisms leading to the development of chronic upper (sino-nasal) airway inflammation has to some extent paralleled investigations of aberrant pathways operant in asthma. In this review, we focus on recent developments in understanding the innate immune pathways as well as adaptive (late) immune responses in CRS and asthma and their implication as potentially modifiable targets in CRS. Specific biologic therapy (that is, monoclonal antibodies targeting cytokines, cytokine receptors, or specific key molecules targeting inflammation) is an exciting proposition for the future of medical management of CRS. As of the writing of this article, the agents described are not approved for use in CRS; many have partial approval for use in asthma or are considered experimental.
Highlights
Recent advances in the biologic therapy of asthma and the potential role of these biologics for chronic rhinosinusitis (CRS) therapy are the focus of this review
It is worth mentioning that currently mepolizumab is Food and Drug Administration (FDA)-approved for treatment of severe asthma with an underlying eosinophilic phenotype but at doses substantially smaller (100 mg) than what clinical studies have typically used
Multiple agents are on the horizon for management of type 2 helper (Th2) type and eosinophil-driven CRS
Summary
Recent advances in the biologic therapy of asthma and the potential role of these biologics for chronic rhinosinusitis (CRS) therapy are the focus of this review. Downstream (late) and adaptive immune pathways and potential targets Given the significant contribution of Th2-mediated inflammation in CRS, especially in eosinophilic CRS or CRSwNP, there is considerable potential for effective blockade of Th2 type cytokines directly to reduce the allergic inflammation. It is worth mentioning that currently mepolizumab is FDA-approved for treatment of severe asthma with an underlying eosinophilic phenotype (eosinophil count greater than 300 cells/mm3) but at doses substantially smaller (100 mg) than what clinical studies have typically used. Other biologicals such as reslizumab (anti-IL-5) or benralizumab (anti-IL-5R) that inhibit IL-5 signaling would be of theoretical benefit due to their ability to inhibit eosinophilic inflammation. The involvement of IL-17 (and IL-22) in some of the subtypes of CRS (both IL-5-negative and IL-5-high groups) suggests the potential applicability of specific use of these agents in specific subgroups[49]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
