Excessive periostin expression and Th2 response in patients with nasal polyps: association with asthma

Abstract

Background: Periostin has been shown to be upregulated in chronic rhinosinusitis with nasal polyps (CRSwNP), especially in the CRSwNP patients with asthma. However, the underlying mechanism that how periostin contributes to the polyp genesis remains unclear.Methods: In this study, we collected 63 CRSwNP patients' nasal polyps (NPs) and 25 control subjects' uncinated tissues. The expressions of periostin, thymic stromal lymphopoietin (TSLP), and other proinflammatory cytokines were examined using IHC staining, qRT-PCR, Western blot (WB), ELISA and FACS. The eosinophil infiltration, phenotype profiles and clinical characteristics of 2 NP subtypes (eosinophilic and non-eosinophilic) were evaluated. We examined the effects and mechanisms of periostin on human nasal epithelial cells cultured at air-liquid interface (ALI).Results: The expressions of periostin in NPs with asthma were higher than without asthma and the control nasal mucosa and positively associated with the TSLP (P<0.05). And the periostin levels was positively associated with the basement membrane thickness, goblet cell hyperplasia and tissue eosinophilia polyp tissues, as well as the clinical parameters (computed tomography scores, polyp size, and polyp recurrence after endoscopic surgery). In vitro experiments show that type 2 T-helper (Th2) cytokines interleukin-4 (IL-4), IL-13 and TGF-β1 stimulates epithelial cells derived from polyp tissues to produce periostin through ERK and STAT6 signal pathways (P<0.05). Autocrine or recombinant periostin activates epithelial cells to produce TSLP via NF-κB signal pathways (P<0.05). The supernatant of periostin-treated epithelial cells activates dendritic cells (DCs), which subsequently induce naïve T cells to differentiate into Th2 cells and express IL-4 and IL-13. Conclusions:Our findings indicate periostin may play an important role in the polyp genesis, which can be considered as a therapeutic target for the management of CRSwNP.

Periostin as a Biomarker of Allergic Inflammation in Atopic Bronchial Asthma and Allergic Rhinitis (a Pilot Study)

“…Among the symptoms, rhinorrhea best correlated with periostin levels (R=0.36; p=0.02). This result is consistent with the available literature in that an increased expression of periostin correlates with an increased activity of the glands of the respiratory tract and an increased volume of their secretion [ 33 , 45 ].…”

“…Furthermore, in children with NM hypertrophy in the medial surface of the conchae, there was significantly more periostin, i.e., 21.6 [10.7; 1516.8] ng/mg; p=0.02. This, however, contradicts the literature data about an increased expression of the gene encoding for periostin and an increase in periostin-protein in sinonasal polyps and systemic bio-substrates [ 30 , 45 , 46 ]. For example, in a study by Asano et al [ 48 ], serum periostin levels in patients with asthma with chronic rhinosinusitis and nasal polyps were significantly higher (130.0±46.6 ng/ml) than in patients without nasal polyps (87.9±37.7 ng/ml); p=0.001.…”

The diagnostic importance of periostin as a biomarker in chronic rhinosinusitis with nasal polyp

“…Wei et al . found that tissue periostin had a significant positive relationship with previous ESS and asthma in 63 CRSwNP patients [ 12 ]. Unlike the literature, our study detected no significant relationship between serum and tissue periostin and asthma in the CRSwNP group ( p > 0.05).…”

“…Preoperative CT can be used for surgical planning, as well as for follow-up and postoperative treatment [ 10 ]. Moreover, some studies positively correlate periostin with the severity of CRSwNP in radiological evaluations [ 11 , 12 ].…”

Airway Epithelial Dynamics in Allergy and Related Chronic Inflammatory Airway Diseases

“…Periostin promotes adhesion and migration of epithelial cells and is associated with CRSwNP (Ishida et al, 2012;Ohta et al, 2014;Laury et al, 2015;Milonski et al, 2015;Shiono et al, 2015;Wang et al, 2015;Ebenezer et al, 2017;Xu et al, 2017;Wei et al, 2018;Yang et al, 2018;Lehmann et al, 2019) and asthma (Carpagnano et al, 2018;Wei et al, 2018). The EMT process is driven by an array of factors such as WNT, reactive oxygen species, proteases, HIF1, IL-13 Epiregulin, Oncostatin M, and IL-1 (Oyer et al, 2013;Batzakakis et al, 2014;Schleimer, 2017;Aazami et al, 2018;Yang et al, 2018;Tomaszewska et al, 2019).…”