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

Abstract

The involvement of periostin in Th2-dependent allergic inflammation has been documented. However, the significance of periostin as a biomarker of local allergic inflammation in the nasal mucosa (NM) of patients with atopic bronchial asthma (BA) and allergic rhinitis (AR) is yet to be determined. The aim of the study was to determine the presence of periostin and evaluate its role as a non-invasive marker of allergic inflammation in the nasal secretions of children with atopic BA and AR. Materials and Methods. In 43 patients aged 4–17 years with atopic BA and AR, the NM was examined using nasal video-endoscopy and (if indicated) computed tomography; the amount of periostin in the nasal secretion was determined by the enzyme immunoassay. Results. Exacerbation of AR was accompanied by a statistically significant increase in the level of periostin in the nasal secretion: up to 0.84 [0.06; 48.79] ng/mg, whereas in remission, that was 0.13 [0.00; 0.36] ng/mg; p=0.04. This value increased progressively as the severity of AR increased from 0.16 [0.00; 0.36] ng/mg in the mild course to 0.20 [0.00; 9.03] ng/mg in AR of moderate severity, and to 10.70 [0.56; 769.20] ng/mg in most severe cases; p=0.048. Hypertrophy or polyposis of the nasal and/or paranasal mucosa was detected in 34.9% (15/43) of the examined patients. The concentration of periostin in the nasal secretion was lower in children without NM hypertrophy: 0.18 [0.001; 4.30] ng/mg vs 0.78 [0.13; 162.10] ng/mg in patients with NM hypertrophy; the differences were close to statistically significant: p=0.051. The level of nasal periostin depended on the clinical form of hypertrophy in the sinonasal mucosa, reaching 0.17 [0.00; 0.32] ng/mg in children with polyposis hyperplasia of NM and 21.6 [10.70; 1516.80] ng/mg — with hypertrophy of the NM in the medial surface of the concha; p=0.02. Conclusion. Exacerbation and increased severity of AR in patients with atopic BA are accompanied by an increased level of periostin in the nasal secretion. This allows us to consider the level of nasal periostin as a biomarker of local allergic inflammation in the NM of patients with atopic BA combined with AR. Hypertrophic changes in the sinonasal mucosa are generally accompanied by an increased level of nasal periostin; specifically, this level significantly depends on the clinical form of mucous membrane hypertrophy and requires additional studies.

Effect of Air Pollutants on Allergic Inflammation in Structural Cells of the Nasal Mucosa

“…In 2011, it was first reported that the serum periostin level could be utilized to predict the efficacy of a monoclonal antibody for severe asthma, and its role as a potential biomarker for type 2 inflammation in allergic diseases has been investigated ever since [ 20 ]. Hoshino et al [ 21 ] reported its utility as a marker of response to sublingual immunotherapy, and Krasilnikova et al [ 22 ] found that the exacerbation of AR was associated with increased periostin levels in nasal secretion.…”

The Relationship Between Indicators of Nasal Respiratory Function and Spirometric Parameters in Children With Bronchial Asthma

“…Small airways may be the most vulnerable and sensitive to both the rhinobronchial reflex and cytokinemia, which are currently being considered as the main mechanisms of the pathological influence of AR/ARS on the course of BA (17). However, this assumption requires further study, which would include the identification of local and systemic biomarkers of inflammation and remodeling (6,(55)(56)(57). Nevertheless, it is worth noticing that our data are consistent with the results of studies by Iyer and Athavale (34), which showed that patients with AR are characterized by a high risk of latent damage to the small respiratory tract.…”

Nasal TSLP and periostin in infants with severe bronchiolitis and risk of asthma at 4 years of age

“…Several cytokines have been involved in Th2-asthma, among them, the alarmins, initiators of T2 inflammation: IL-33, IL-25, and thymic stromal lymphopoietin (TSLP). Alarmins promote the expression of IL-4, IL-5, and IL-13 and increase the levels of periostin [ 8 ].…”