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Updated: Apr 17, 2026
Absorption of Nasal and Bronchial Fluids: Precision Sampling of the Human Respiratory Mucosa and Laboratory Processing of Samples
Published on: January 21, 2018
Immune profile modulation of blood and mucosal eosinophils in nasal polyposis with concomitant asthma
Geoffrey Mortuaire1, Isabelle Gengler2, Claire Vandenhende-Szymanski2
1INSERM U995, Université de Lille, Lille, France; EA 2686, Université de Lille, Lille, France; Department of Otorhinolaryngology-Head and Neck Surgery, University Hospital, Lille, France; French Eosinophil Network, University Hospital, Lille, France.
Background:
Chronic rhinosinusitis with nasal polyps (CRSwNP) is frequently associated with asthma. Mucosal eosinophil (EO) infiltrate has been found to correlate with asthma and disease severity but not necessarily in every patient. Other multifactorial immune processes are required to determine disease endotypes and response to treatment.
Objective:
To evaluate EO immunomodulation for migration and survival in accordance with inflammatory protein profiles and asthmatic status in CRSwNP.
Methods:
Ninety-three patients (47 with asthma) with CRSwNP were included. Each patient was staged clinically according to symptom severity and polyp size. Nasal secretions were collected to establish a cytokine profile. The EOs were purified from blood samples and nasal polyps to delineate specific immunophenotypes by flow cytometry and determine in vitro EO survival in relation to asthmatic status.
Results:
The CRSwNP in patients with asthma was characterized by eosinophilia and a high level of interleukin (IL)-5 in nasal secretions. Although EOs exhibited activation profiles after mucosal migration, there was relative down-expression of IL-5 receptor-α (IL-5Rα) on nasal EOs in patients with asthma. The EO culture with IL-5 and IL-9 showed an antiapoptotic effect in patients with asthma through IL-5Rα modulation.
Conclusion:
Mucosal eosinophilia seems to be induced by EO nasal trapping through modulation of adhesion receptors. In patients with asthma, EO involvement is enhanced by the antiapoptotic synergistic action of T-helper cell type 2 cytokines on IL-5Rα expression. This study shows for the first time that IL-9 is involved in EO homeostasis in CRSwNP and could explain the low benefit of anti-IL-5 therapy for some patients with asthma and nasal polyposis.
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