• Innate Immunity
• Airway Epithelium
• Neutrophil Biology

Chronic rhinosinusitis (CRS) is a heterogenous airways disease characterised by inflammation of the upper airways and sinuses that persists for at least 12 weeks. CRS is frequently divided into two endotypes based on the presence or absence of nasal polyps (NPs): CRS with NPs (CRSwNP) and CRS without NPs (CRSsNP). Inflammatory patterns in the two groups are different and studies indicate that CRSsNP is dominated by a type 1 inflammatory profile associated with increased interferon (INF)-γ and tumour necrosis factor (TGF)-β expression and neutrophilic inflammation.1 By comparison, type 2 inflammatory responses characterised by interleukin (IL) 4, IL-5, IL-13 cytokine expression and eosinophilic inflammation are features of CRSwNP.1 This categorisation may, however, be oversimplified as recent studies show that this may be subject to racial and regional differences.2 ,3 While the majority of Caucasian patients sampled in the USA and Europe have a pronounced infiltration of eosinophils and expression of IL-5 in the NPs, patients with CRSwNP in East Asian countries including Japan, Korea and China, exhibit a mixed inflammatory profile. About half the Asian patients with CRSwNP exhibit an eosinophilic chronic rhinosinusitis (ECRS) while the rest have a non-eosinophilic more neutrophilic or mixed inflammatory chronic rhinosinusitis (non-ECRS) characterised by type 1 dominant inflammation. Although a number of hypotheses have been proposed regarding the pathogenesis of CRSwNP, the precise molecular mechanisms remain unclear and likely lie beyond rudimentary clinical classifications of CRS. An emphasis on defining CRS endotypes based on distinct functional or pathobiological mechanisms of disease may be more effective at identifying patient groups that would respond to therapeutic interventions targeting specific proinflammatory mediators or infectious agents that trigger the disease pathology.

The inflammatory profile of CRSsNP is largely type 1, although there are discrepancies over which isoforms of TGF-β are increased per se and in what …