Presentation: Increased Expression of Filaggrin, TSLP, Periostin, IL13 and IL-33 in Nasal Polyps ( World Allergy Congress)

Thursday, 15 October 2015

Hall D1 Foyer (Floor 3) (Coex Convention Center)

Liang Zhang, MD , Dept. of Pediatrics, Nippon Medical School, Tokyo, Japan

Ruby Pawankar, MD, Ph.D, FRCP, FAAAAI , Div of Allergy, Department of Pediatrics, Nippon Medical School, Tokyo, Japan

So Watanabe, MD, PhD , Department of Otorhinolaryngology, Showa University School of Medicine, Tokyo, Japan

Manabu Nonaka, MD, Ph.D , Dept. of Otolaryngology, Tokyo Women’s Medical University, Tokyo, Japan

Miyuki Hayashi, MD, Ph.D , Dept. of Pediatrics, Nippon Medical School, Tokyo, Japan

Shingo Yamanishi, MD, Ph.D , Dept. of Pediatrics, Nippon Medical School,, Tokyo, Japan

Harumi Suzaki, MD, PhD , Nasal. PNS Disease and Allergy Institute, Tokyo General Hospital, Tokyo, Japan

Hitome Kobayashi, MD, Ph.D , Otolarylgology, Showa University School of Medicine, Tokyo, Japan

Yasuhiko Itoh, MD, Ph.D , Dept of Pediatrics, Nippon Medical School,, Tokyo, Japan

Purpose:

Chronic rhinosinusitis (CRS), with nasal polyposis is a chronic inflammatory disease of the upper airways often associated with asthma and characterized by markedly increased numbers of eosinophils, Th2 type lymphocytes, fibroblasts, goblet cells and mast cells. The inflammation leads to a proliferative response in the extracellular matrix (ECM). Periostin is an ECM protein known to play a role in tissue remodeling in inflammatory diseases of the upper and lower airways. Furthermore epithelial-derived genes such as filaggrin have been highlighted in asthma or atopic dermatitis (AD) or both via its role in barrier function. Here we investigated the expression of periostin and filaggrin in nasal polyps (NP) from atopics and non-atopics in comparison with the nasal mucosa from patients with allergic rhinitis (AR) and its potential role in nasal polyposis.

Methods:

Nasal polyp specimens and biopsies of nasal mucosa were obtained at surgery as part of the treatment for removal of NP or for hypertrophied turbinates. Immunoreactivity for periostin, TSLP, filaggrin and IL-13 in NP from atopic and non-atopic patients and in the nasal mucosa of patients with AR was analyzed by immunohistochemistry using the peroxidase-based Avidin-Biotin Complex (ABC) method. Cell counts were analyzed using an objective micrometer and the density of immunoreactivity was quantified by Image J analysis system. Real Time PCR was done for analyzing the mRNA expression of IL-33

Results:

Filaggrin immunoreactivity was detected in epithelial cells and inflammatory cells. The number of Filaggrin+ cells in the epithelium of patients with NP was significantly higher than that in the nasal mucosa of the AR patients. The number of filaggrin+ cells in the lamina propria of patients with NP was significantly higher than that in the nasal mucosa of the AR patients. There was no difference in the number of filaggrin+ cells between nasal polyps from atopic and non-atopic patients. Periostin immunoreactivity was mainly detected in the basement membrane and the density of immunoreactivity of periostin in NP was significantly higher in NP than in the nasal mucosa of the AR patients. TSLP was detected in epithelial cells and in immune cells and greater in NP than AR mucosa. There was no difference in the density of immunoreactivity of periostin between NP from atopic and non-atopic patients. IL-13+ cells and IL-33 expression were also higher in NPs and there was a good correlation between the IL-13+ cells and periostin

Conclusions:

Based on our previous findings of the high levels of IL-13 and TGF-beta in NP and the present findings of the increased expression of filaggrin and periostin in NP irrespective of the atopic status, filaggrin may potentially play a role in the barrier function and periostin may play a role

2050 Increased Expression of Filaggrin, TSLP, Periostin, IL13 and IL-33 in Nasal Polyps