Impact of chronic rhinosinusitis on severe asthma patients

Abstract

Coexistence of chronic rhinosinusitis (CRS) with asthma appears to impair asthma control. Type-2 innate lymphoid cells (ILC2s) respond to the cytokines of thymic stromal lymphopoietin (TSLP), interleukin (IL)-25 and IL-33, thus contributing to airway diseases such as CRS and asthma. We investigate whether the augmented Th2-cytokines in CRS might be related to sinonasal tract ILC2s corresponding to enhanced IL-25, IL-33 and TSLP release in severe asthmatics, and be involved in asthma control. Twenty-eight asthmatics (12 non-severe and 16 severe) with CRS receiving nasal surgery were enrolled. The predicted FEV1 inversely associated with CRS severity of CT or endoscopy scores. Higher expression of Th2-driven cytokines (IL-4, IL-5, IL-9, and IL-13), TSLP, IL-25 and IL-33 in nasal tissues was observed in severe asthma. Severe asthmatics had higher ILC2 cell counts in their nasal tissues. ILC2 counts were positively correlated with Th2-cytokines. Nasal surgery significantly improved asthma control and lung function decline in severe asthma and CRS. The higher expression of IL-33/ILC2 axis-directed type 2 immune responses in nasal tissue of CRS brought the greater decline of lung function in severe asthma. ILC2-induced the upregulated activity of Th2-related cytokines in asthmatics with CRS may contribute to a recalcitrant status of asthma control.

Association of nasal microbiome and asthma control in patients with chronic rhinosinusitis

“…Uncontrolled upper airway inflammation in the context of CRS is associated with lower airway T-helper-2 mediated inflammation and recalcitrant asthma, however; the underlying mechanism of this link is rather complicated and currently under investigation. (2) Rhinosinusitis is also linked to increased asthma severity and exacerbation rate. (3) Nevertheless, fundamental questions regarding the mechanisms of chronic mucosal inflammation in CRS, and how chronic sinonasal inflammation may affect the lower airways remain unanswered.…”

Novel innate and adaptive lymphocytes: The new players in the pathogenesis of inflammatory upper airway diseases

“…In asthmatic patients with concomitant CRS, the activation of IL-33/ILC2 axis in nasal mucosa was associated with decline of lung function and recalcitrant status of asthma control, suggesting an important role of nasal ILC2 activation in worsening asthma. 51 Interestingly, corticosteroid treatment is able to induce apoptosis of ILC2s and diminish the accumulation of ILC2s in nasal polyps, which is accompanied by resolution of inflammation. 46 The studies of AR mainly focus on circulating ILC2s.…”

“…In addition, the expression of epithelial cell‐derived IL‐25, IL‐33 and TSLP has been found up‐regulated in nasal polyps, highlighting an ILC2 favouring local milieu in CRSwNP. In asthmatic patients with concomitant CRS, the activation of IL‐33/ILC2 axis in nasal mucosa was associated with decline of lung function and recalcitrant status of asthma control, suggesting an important role of nasal ILC2 activation in worsening asthma . Interestingly, corticosteroid treatment is able to induce apoptosis of ILC2s and diminish the accumulation of ILC2s in nasal polyps, which is accompanied by resolution of inflammation …”

Impact of cigarette smoke and IL-17A activation on asthmatic patients with chronic rhinosinusitis

“…Chronic rhinosinusitis (CRS) is frequently associated with asthma (1) , and its presence is related to asthma severity. Among patients with asthma and CRS, pulmonary function and asthma control were closely related to the severity of nasal symptoms (2) .…”