Immunological mechanisms underlying chronic rhinosinusitis with nasal polyps

Introduction: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a common and quality-of-life impacting disorder, with an underlying immunological mechanism similar to other conditions such as eosinophilic asthma or atopic eczema.

Areas covered: This review article summarizes the most recent evidence on the main immunological mechanisms involved in the pathogenesis and the perpetuation of CRSwNP, with a particular focus on the key role of epithelium-derived inflammation as a consequence of the interaction with the airborne environment.

Expert commentary: The increase in knowledge of the immunology of CRSwNP leads to the development of therapeutical strategies based upon the use of biologic agents that, according to a personalized and precision medicine approach, will provide each single patient with the most suitable immunological treatment.     

United airways again: high prevalence of rhinosinusitis and nasal polyps in bronchiectasis

Background: Although various relationships between the lower and upper airways have been found, the association of bronchiectasis with chronic rhinosinusitis and nasal polyps has not been thoroughly evaluated. This study was undertaken to examine the association of idiopathic and postinfective bronchiectasis with chronic rhinosinusitis and nasal polyposis. Methods: In a prospective study, 56 patients with idiopathic and 32 with postinfective bronchiectasis were evaluated for chronic rhinosinusitis and nasal polyposis by using EP³OS criteria and assessing: symptoms score, nasal endoscopy, sinonasal and chest CT scan, nasal and lung function and nasal and exhaled NO. Results: Most bronchiectasis patients (77%) satisfied the EP³OS criteria for chronic rhinosinusitis, with anterior (98.5%) and posterior (91%) rhinorrhea and nasal congestion (90%) being the major symptoms. Patients presented maxillary, ethmoidal and ostiomeatal complex occupancy with a total CT score of 8.4 ± 0.4 (0–24). Using endoscopy, nasal polyps with a moderate score of 1.6 ± 0.1 (0–3) were found in 25% of patients. Nasal NO was significantly lower in patients with nasal polyposis (347 ± 62 ppb) than in those without them (683 ± 76 ppb; P < 0.001), and inversely correlated (R = ?0.36; P < 0.01) with the ostiomeatal complex occupancy. In the chest CT scan, patients with chronic rhinosinusitis showed a higher bronchiectasis severity score (7.2 ± 0.5; P < 0.001) than patients without (3.7 ± 0.7). The prevalence of chronic rhinosinusitis, nasal polyps and other outcomes were similar in idiopathic and postinfective bronchiectasis. Conclusions: The frequent association of chronic rhinosinusitis and nasal polyposis with idiopathic and postinfective BQ supports the united airways concept, and it suggests that the two type of bronchiectasis share common etiopathogenic mechanisms.     

Chronic rhinosinusitis with nasal polyps: insights into mechanisms of disease from emerging biological therapies

Introduction: Chronic rhinosinusitis with nasal polyps (CRSwNP) is a complex disease of the upper airway, with long-term morbidity. With detailed mechanistic studies currently lacking, understanding of the immunopathogenesis is still limited. However, outcomes from CRSwNP clinical studies using biologics that block key mediators or cells may provide some insights into how immune signaling pathways potentially integrate and modulate each other and contribute to disease. Current treatments are often ineffective and there is an urgent unmet clinical need for effective therapeutic strategies. Emerging biologics hold promise.

Areas covered: This review covers the biology of CRSwNP in terms of the clinical outcomes reported from blocking immune cascades with available biologics. Immune amplification mechanisms and how biologics can potentially modulate such ‘master’ cytokines and signaling proteins that drive inflammation and contribute to tissue remodeling in CRSwNP are discussed.

Expert commentary: Biologics have the potential to transform CRSwNP treatment. The ability to predict clinical response in a complex disease as CRSwNP to a biologic cannot necessarily be predicted by measuring a single protein or cell as a biomarker of disease. Further studies with biologics must be carefully undertaken to fully evaluate wider biomarker associated pheno-endotype responses along with any associated asthma outcome measures.