Objectives/hypothesis: Several genes have been reported to be upregulated in human nasal polyps in previous genetic analyses. Among these genes, periostin is known to be overexpressed in nasal polyps obtained from aspirin-sensitive patients. Using periostin-null mice, we investigated the role of periostin in a murine model of eosinophilic rhinosinusitis with nasal polyps.
Study design: Animal study.
Methods: Eosinophilic rhinosinusitis was induced in both periostin-null and wild-type mice according to previously established protocols. In brief, ovalbumin (OVA) was used for sensitization and prolonged intranasal stimulation. Staphylococcus aureus enterotoxin B was applied intranasally to develop polyplike lesions. To examine the inflammation and mucosal lesions, hematoxylin and eosin, Sirius red, and Giemsa staining were performed.
Results: There was no definite difference in the maximal mucosal thickness between periostin-null and wild-type mice. In contrast, some parameters of inflammation, including the number of polyplike lesions and mast cells, were aggravated in the periostin-null mice compared to wild type. Eosinophilic infiltration was aggravated in the OVA-stimulated periostin-null mice, compared to OVA-stimulated wild-type mice, whereas there was no apparent difference between wild-type and periostin-null mice challenged with additional S aureus enterotoxin B.
Conclusions: The loss of periostin appears to enhance polyplike lesion formation and mast cell infiltration in a mouse model of eosinophilic rhinosinusitis with nasal polyps.
Copyright © 2013 The American Laryngological, Rhinological, and Otological Society, Inc.