Rhinitis, sinusitis, and upper airway diseaseDefective epithelial barrier in chronic rhinosinusitis: The regulation of tight junctions by IFN-γ and IL-4
Section snippets
Patients
Patients undergoing paranasal sinus surgery because of CRS with and without nasal polyposis were enrolled as study patients. Patients undergoing paranasal sinus surgery for noninflammatory reasons (ie, cerebrospinal fluid leak, bullous middle turbinate, and those undergoing septal surgery) were used as healthy control subjects. Nasal or systemic corticosteroid administration up to 4 weeks before surgery was considered an exclusion criterion. Patients with CRS caused by underlying systemic
Disrupted epithelial integrity and TJs in patients with CRS
We first investigated whether there is any difference in tissue resistance in patients with CRS. Large and intact biopsy specimens were used for resistance assessments in an Ussing chamber to quantify the epithelial integrity directly in affected tissues. The measurement revealed significantly (P = .03) higher trans-tissue resistances in control subjects (105.8 ± 6.4 Ω × cm2) compared with that seen in patients with CRSwNP (48.8 ± 9.6 Ω × cm2). Samples from patients with CRSsNP (81.5 ± 7.9
Discussion
The present study analyzes the function and expression of TJs in patients with CRS. We provide direct in vivo evidence for a defective barrier function in patients with CRSwNP in conjunction with a decreased expression of TJ proteins and mRNA levels compared with that seen in control subjects. Thus far, most of the research has focused on the inflammatory pathomechanisms and identification of proinflammatory mediators in patients with CRS rather than on the effects on the nasal/paranasal sinus
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Cited by (0)
The laboratory of C.A.A. is supported by the European Allergy and Asthma Center Davos (EACD), Swiss National Science Foundation grants 32-132899 and 32-112306, the Christine Kühne Center for Allergy Research and Education (CK-CARE), the Müller-Gierok-Foundation, and University Hospital Zurich.
Disclosure of potential conflict of interest: M. B. Soyka has received research support from the Müller-Gierok Foundation, the European Allergy and Asthma Center Davos, the Swiss National Foundation, University Hospital Zurich, and CK-CARE and is employed by University Hospital Zurich. C. A. Akdis has received research support from Novartis, PREDICTA, the Swiss National Science Foundation, MeDALL, the Global Allergy and Asthma European Network, and CK-CARE; has provided legal consultation/expert witness testimony on the topics of Acellion TH2-specific receptors, Aventis T-cell Bell regulation, and allergen-specific immunotherapy (for Stallergenes and Allergopharma); is president of the European Academy of Allergy and Clinical Immunology, a GA2LEN ex-committee member, director of CK-CARE, and a fellow and interest group member for the American Academy of Allergy, Asthma & Immunology. The rest of the authors declare that they have no relevant conflicts of interest.