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Review
. 2021 Mar 24;22(7):3340.
doi: 10.3390/ijms22073340.

Asthma and Chronic Rhinosinusitis: How Similar Are They in Pathogenesis and Treatment Responses?

Andrea Matucci  1 , Susanna Bormioli  1 , Francesca Nencini  1 , Fabio Chiccoli  2 , Emanuele Vivarelli  1 , Enrico Maggi  3 , Alessandra Vultaggio  1
Affiliations
Review

Asthma and Chronic Rhinosinusitis: How Similar Are They in Pathogenesis and Treatment Responses?

Andrea Matucci et al. Int J Mol Sci. .

Abstract

Severe asthma and rhinosinusitis represent frequent comorbidities, complicating the overall management of the disease. Both asthma and chronic rhinosinusitis (CRS) can be differentiated into endotypes: those with type 2 eosinophilic inflammation and those with a non-type 2 inflammation. A correct definition of phenotype/endotype for these diseases is crucial, taking into account the availability of novel biological therapies. Even though patients suffering from type 2 severe asthma-with or without CRS with nasal polyps-significantly benefit from treatment with biologics, the existence of different levels of patient response has been clearly demonstrated. In fact, in clinical practice, it is a common experience that patients reach a good clinical response for asthma symptoms, but not for CRS. At first glance, a reason for this could be that although asthma and CRS can coexist in the same patient, they can manifest with different degrees of severity; therefore, efficacy may not be equally achieved. Many questions regarding responders and nonresponders, predictors of response, and residual disease after blocking type 2 pathways are still unanswered. In this review, we discuss whether treatment with biological agents is equally effective in controlling both asthma and sinonasal symptoms in patients in which asthma and chronic rhinosinusitis with nasal polyps coexist.

Keywords: asthma; biological agents; chronic rhinosinusitis; nasal polyps; type 2 inflammation.

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Figure 1
Figure 1
Chronic eosinophilic type 2 inflammatory process at the bronchial wall level of asthmatic patients, both allergic and non, leads to airway remodeling characterized by epithelial damage, goblet cell hyperplasia, subepithelial collagen deposition, airway smooth muscle hyperplasia and increased vascularity (A); in allergic rhinitis, despite type 2 inflammation is a disease hallmark, remodeling does not occur (B); in CRS type 2 inflammation occurs leading to the development of nasal polyps (CRSwNP), in which the remodeling process is characterized by more evident pseudocyst formation, stromal edema and collagen deposition (C); in CRSsNP type 1/3 neutrophilic inflammation is driving force in which remodeling is more evident due to basal membrane thickening, fibrosis and goblet cells hyperplasia (D).
Figure 2
Figure 2
The mAb concentration at bronchial and nasal levels can be influenced by several factors, such as subcutaneous absorption, lymphatic transportation and different blood perfusion in the different organs and tissues, all conditioned by the chronic inflammatory process.
See this image and copyright information in PMC

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