Goblet cell hyperplasia as a feature of neutrophilic asthma.


Journal

Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology
ISSN: 1365-2222
Titre abrégé: Clin Exp Allergy
Pays: England
ID NLM: 8906443

Informations de publication

Date de publication:
06 2019
Historique:
received: 09 07 2018
accepted: 06 12 2018
pubmed: 3 2 2019
medline: 31 7 2020
entrez: 3 2 2019
Statut: ppublish

Résumé

Goblet cell hyperplasia (GCH) is a pathological finding classically reported across asthma severity levels and usually associated with smoking. Multiple biological mechanisms may contribute to excessive mucus production. We aimed to decipher the clinical meanings and biological pathways related to GCH in non-smokers with asthma. Cough and sputum assessment questionnaire (CASA-Q) responses at entry and 1 year later were compared to clinical and functional outcomes in 59 asthmatic patients. GCH was assessed through periodic-acid shift (PAS) staining on endobronchial biopsies obtained at entry in a subset of 32 patients. Periodic-acid shift-staining analysis revealed a double wave distribution discriminating patients with (>10% of the epithelial area) or without GCH. CASA-Q scores were mostly driven by overall asthma severity (P < 0.0001). CASA-Q scores remained stable at 1 year and were independently associated with BAL eosinophil content irrespective of the presence of GCH. GCH was unrelated to the presence of bronchiectasis at CT, GERD or chronic rhinosinusitis, but correlated well with neutrophilic inflammatory patterns observed upon BAL cellular analysis (P = 0.002 at multivariate analysis). BALF bacterial loads were unrelated to GCH or to CASA-Q. Goblet cell hyperplasia is disconnected from chronic cough and sputum when assessed by a specific questionnaire. GCH is related to neutrophilic asthma whereas symptoms are related to airway eosinophilia. The clinical counterpart of GCH is unlikely assessed by the CASA-Q.

Sections du résumé

BACKGROUND
Goblet cell hyperplasia (GCH) is a pathological finding classically reported across asthma severity levels and usually associated with smoking. Multiple biological mechanisms may contribute to excessive mucus production.
OBJECTIVE
We aimed to decipher the clinical meanings and biological pathways related to GCH in non-smokers with asthma.
METHODS
Cough and sputum assessment questionnaire (CASA-Q) responses at entry and 1 year later were compared to clinical and functional outcomes in 59 asthmatic patients. GCH was assessed through periodic-acid shift (PAS) staining on endobronchial biopsies obtained at entry in a subset of 32 patients.
RESULTS
Periodic-acid shift-staining analysis revealed a double wave distribution discriminating patients with (>10% of the epithelial area) or without GCH. CASA-Q scores were mostly driven by overall asthma severity (P < 0.0001). CASA-Q scores remained stable at 1 year and were independently associated with BAL eosinophil content irrespective of the presence of GCH. GCH was unrelated to the presence of bronchiectasis at CT, GERD or chronic rhinosinusitis, but correlated well with neutrophilic inflammatory patterns observed upon BAL cellular analysis (P = 0.002 at multivariate analysis). BALF bacterial loads were unrelated to GCH or to CASA-Q.
CONCLUSIONS AND CLINICAL RELEVANCE
Goblet cell hyperplasia is disconnected from chronic cough and sputum when assessed by a specific questionnaire. GCH is related to neutrophilic asthma whereas symptoms are related to airway eosinophilia. The clinical counterpart of GCH is unlikely assessed by the CASA-Q.

Identifiants

pubmed: 30710420
doi: 10.1111/cea.13359
doi:

Types de publication

Clinical Trial Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

781-788

Informations de copyright

© 2019 John Wiley & Sons Ltd.

Auteurs

Khuder Alagha (K)

Département de Pneumologie et Addictologie, University of Montpellier, Montpellier, France.
Aix Marseille University, INSERM, INRA, C2VN, Marseille, France.

Arnaud Bourdin (A)

Département de Pneumologie et Addictologie, University of Montpellier, Montpellier, France.
PhyMedExp, Hôpital Arnaud de Villeneuve, INSERM U1046, CNRS, UMR 9214, University of Montpellier, Montpellier, France.
CHU Montpellier, Montpellier, France.

Charlotte Vernisse (C)

PhyMedExp, Hôpital Arnaud de Villeneuve, INSERM U1046, CNRS, UMR 9214, University of Montpellier, Montpellier, France.
CHU Montpellier, Montpellier, France.

Céline Garulli (C)

Aix Marseille University, INSERM, INRA, C2VN, Marseille, France.

Céline Tummino (C)

Clinique des Bronches, Allergies et Sommeil, Hôpital Nord, AP-HM, Aix Marseille Université Marseille, Marseille, France.

Jérémy Charriot (J)

Département de Pneumologie et Addictologie, University of Montpellier, Montpellier, France.

Isabelle Vachier (I)

Département de Pneumologie et Addictologie, University of Montpellier, Montpellier, France.

Carey Suehs (C)

Département de Pneumologie et Addictologie, University of Montpellier, Montpellier, France.

Pascal Chanez (P)

Aix Marseille University, INSERM, INRA, C2VN, Marseille, France.
Clinique des Bronches, Allergies et Sommeil, Hôpital Nord, AP-HM, Aix Marseille Université Marseille, Marseille, France.

Delphine Gras (D)

Aix Marseille University, INSERM, INRA, C2VN, Marseille, France.

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