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Table of Contents
ORIGINAL ARTICLE
Year : 2018  |  Volume : 67  |  Issue : 1  |  Page : 4-8

Role of serum periostin as a biomarker in diagnosis of bronchial asthma


1 Department of Clinical Pathology, Tanta Fever Hospital, Tanta, Egypt
2 Department of Clinical Pathology, Faculty of Medicine, Tanta University, Tanta, Egypt
3 Department of Chest, Faculty of Medicine, Tanta University, Tanta, Egypt

Date of Submission02-Oct-2017
Date of Acceptance30-Nov-2017
Date of Web Publication21-Mar-2018

Correspondence Address:
Ibrahim S Ibrahim
Chest Department, Faculty of Medicine, Tanta University, Tanta, 111134
Egypt
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/ejcdt.ejcdt_4_17

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  Abstract 


Background Asthma is a chronic airway disease that is characterized by persistant airway inflammation and remoldeing with bronchial hyperactivity in resulted from one allergen or more leading to episodic airflow obstruction. Periostin can be detected in serum of asthmapatients which largly reflected to its level production in airway. Periostin is secreted by airway epithlialcellin response to iL-13 stimulation and easly leak into the airway capillary. Serum periostin could be aperdector ofairway esinophilliato patients with severeasthma.
Aim of the work Is estimating the serum periostin level in patients with bronchial asthma to evaluate its role in diagnosis.
Methodology This study was carried out on 25 normal healthy individual serveing as control (Group I), 25 patients diagnosed as atopic asthmatic patient regarding to skin prick test (its postive>3) (Group II) and 25 patients diagnosed as non-atopic asthmatic patient regarding to skin prick test (its negative <3) (Group III). Informed consent was taken from all patients and controls. Patient was submitted to full History taking, Clinical evaluation, Chest X-ray, Pulmonary function tests, Skin prick test to inhalant allergens and laboratory investigations including (CBC and Serum levels of periostin were assayed using an enzyme-linked immunosorbent assay (ELISA).
Results Statistical analysis of the results of present work showed that serum periostin was significantly higher in asthmatic group (atopic and non atopic) in comparison to control group. Serum perioestin was also significantly higher in group 11 (atopic asthma) than group 111 (non atopic asthma) as cutting off was>420 and sensitivity and specifity was 40.0, 100.0 resepctivily.
Conclusion Serum periostin can be used in dignosis of asthma and differntiation of atopic asthma from non atopic asthma.

Keywords: atopic asthma, non-atopic asthma, periostin


How to cite this article:
Mohammed DR, Abdelnaby AY, El Zamran EA, Ibrahim IS. Role of serum periostin as a biomarker in diagnosis of bronchial asthma. Egypt J Chest Dis Tuberc 2018;67:4-8

How to cite this URL:
Mohammed DR, Abdelnaby AY, El Zamran EA, Ibrahim IS. Role of serum periostin as a biomarker in diagnosis of bronchial asthma. Egypt J Chest Dis Tuberc [serial online] 2018 [cited 2020 Apr 3];67:4-8. Available from: http://www.ejcdt.eg.net/text.asp?2018/67/1/4/228136




  Introduction Top


Asthma is a chronic disease of airways that affect people all over the world. Asthma is characterized by persistent inflammation and remolding of airway with associated bronchial hyperactivity in response to one or more allergen, resulting in episodic obstruction of airflow [1].

Periostin is a protein that is expressed in extracellular matrix of fibroblasts or epithelial cells. Periostin expression is induced in fibroblasts by T-helper cell type 2 (Th2) cytokines, which may cause subepithelial fibrosis in asthma [2]. In the bronchial epithelial cells of children with asthma, there is significant periostin expression [3], and it is reported that levels of serum periostin could be a biomarker of eosinophilic inflammation of the airways in severe asthma in adults [4].

Many types of cells such as epithelial cells, fibroblasts, and eosinophils express periostin under rest conditions [5]. However, the pattern of expression can be altered in case of inflammation. Periostin expression increased in smooth muscle, the airway epithelium, and inflammatory cells.

Signature molecules of these two types of asthma, finding that periostin as well as serpin peptidase inhibitor, and chloride channel regulator 1, clade B, member 2 is a ‘Th2-high’ asthma signature molecule. The pathological role of periostin in asthma has not yet been established. Several initial studies using periostin-deficient mice showed that periostin acts as a protective molecule against allergic airway inflammation [6].

However, it has been recently reported that periostin accelerates allergic airway inflammation, using periostin-deficient mice and neutralizing antibodies against periostin [7]. The change in pulmonary functions of 20 patients with asthma more than 20 years after they were first diagnosed with asthma was analyzed. The degree of periostin deposition in biopsy samples obtained when they were diagnosed 20 years ago is inversely associated with their subsequent change in pulmonary function, which supports the idea that periostin is an accelerator for bronchial asthma [8].


  Aim Top


The goal of this study was to estimate the serum periostin level in patients with bronchial asthma to evaluate its role in diagnosis.


  Patients and methods Top


This was an observant prospective study that was conducted at Tanta University Hospital, Clinical Pathology and Chest Departments for at least 6 months. The study was approved by the ethical committee of faculty of medicine Tanta University.

The study population was divided into the following:
  1. Group I: 25 normal healthy individuals as control.
  2. Group II: 25 patients diagnosed as having atopic asthma.
  3. Group III: 25 patients diagnosed as having nonatopic asthma.


Inclusion criteria were patients with history of bronchial asthma with reversible airway obstruction. Exclusion criteria were patients with other concomitant chest diseases (chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis), patients with chest infection, patients with malignancy, and patients with cardiac diseases.

Patients were subjected to the following assessments.

Full history taking

Full history included smoking history, exposure to pet animals, special reference to upper airway symptoms, use of inhaled corticosteroids, and any history of sensitization in family.

Clinical evaluation

Thorough clinical examination of the chest by auscultation was done to detect symptoms such as wheezing, difficulty in taking a deep breath, and chest tightness that suggest asthma.

Chest radiography

It is important to detect causes of wheezing or complications and the minor importance of wheezing in the diagnosis of asthma and exacerbations.

Pulmonary function tests

Pulmonary function tests included spirometry to estimate the forced vital capacity (FVC), which measures the exhalation ability as fast and hard as possible after deep inspiration, and the forced expiratory volume (FEV1), which measures the expired volume during the first second of FVC.

Skin prick test to inhalant allergens

According to standard methods with allergens, histamine-positive and negative controls purchased from Creative Drug Industries [9].

Methodology

Sampling: venous blood samples were collected, and complete blood count and absolute eosinophil counts were measured. Serum aliquots were stored at 20°C till the time of measurement of periostin by enzyme-linked immunosorbent assay.

Serum periostin

Serum periostin levels were assayed using enzyme-linked immunosorbent assay (double-antibody sandwich technique, USA) R&D systems (catalog number: MOSF20) that measures the level of sample periostin by adding it to precoated well with human periostin monoclonal antibody and then incubated. Biotin-labeled periostin antibodies were added to form immune complex when combined with streptavidin-horseradish peroxidase, and then the excess uncombined enzyme was remove by washing. When chromogen solutions A and B were added, a blue color was produced by the effect of acid, which is lastly changed into yellow on adding stop solution. The concentration of human periostin in the sample was correlated positively with the intensity of color ([Table 3]).
Table 3 Comparison between the studied groups regarding serum periostin

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  Results Top


This table shows that skin prick test (SPT) was positive in group II and negative in group III; there was a highly significance differences between the two groups regarding SPT, with P value of less than 0.001 ([Figure 1], [Table 1]).
Figure 1 Comparison between the studied groups regarding skin prick test.

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Table 1 Comparison between atopic asthma and nonatopic asthma regarding skin prick test

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This table shows that eosinophils were higher in patient groups than control, as there was a significance differences among the three groups (P<0.001) ([Figure 2], [Table 2]).
Figure 2 Comparison between the studied groups regarding eosinophil (ml).

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Table 2 Comparison between the three studied groups regarding eosinophil (×103/ml)

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This table shows that serum periostin level was higher in group II followed by group III, with lower level in control group; this shows that there were significant differences among the three groups (control, atopic, and nonatopic) regarding serum periostin (P<0.001) ([Figure 3], [Table 3] and [Table 4]).
Figure 3 Comparison between the studied groups according to serum periostin.

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Table 4 Correlation between serum periostin and the studied parameters.

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This table shows that there was insignificance correlation between age and BMI and serum periostin level (P= 0.505 and 0.757, respectively), but there was highly significance correlation between FEV1%, FEV1/FVC%, peak expiratory flow (PEF%), and eosinophil count and serum periostin level (P=0.002, 0.001, <0.001, and <0.001, respectively) ([Figure 4] and [Figure 5]).
Figure 4 Significant correlation between serum periostin and FEV1/FVC%. FEV, forced expiratory volume; FVC, forced vital capacity.

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Figure 5 Significant correlation between serum periostin and eosinophil.

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  Discussion Top


The goal of this study was to evaluate the role of serum periostin as a biomarker in diagnosis of asthma. Patients were divided into three groups. Group I included 25 normal healthy individuals who served as control, group II included 25 patients diagnosed as having nonatopic asthma, and group III included 25 patients diagnosed as having atopic asthma.

In the present study, it was found that family history was significant in patients with asthma (P<0.001). Regarding the uses of inhaled corticosteroids (ICS) and oral corticosteroids, family history was significant in group II (atopic asthma group) and group III (nonatopic asthma group), with P value less than 0.001 and 0.013, respectively.

ICSs are the antiasthmatic drugs of choice. Although ICSs are effective for most patients, 5–10% are resistant or hyporesponsive to them [10],[11]. It is confirmed that inhaled corticosteroids suppress airway inflammation and components of airway remodeling in bronchial asthma.

SPT is an effective test to detect type I allergic reactions that are immunoglobulin E mediated such as atopic asthma, allergic rhinitis, and food allergy. SPTs are done to diagnose allergic sensitivity and applied for use of immunotherapy as the therapeutic modality [9].

In this study, we found that the SPT was positive in group III (nonatopic asthma group) and negative in group II (atopic asthma group); there was a highly significant difference between the two groups regarding SPT (P<0.001).

In our study, we found that eosinophil count was higher in patient groups than control, as there were significance differences among the three groups (P<0.001).

In agreement with these result, Inoue et al. [12] found that there were highly significant differences between patients and control groups regarding blood eosinophil, as it was higher in patient groups (P<0.001) [12].

Results of this study revealed that serum periostin level was higher in group II (atopic asthma group) followed by group III (nonatopic asthma group), with lower level in control group; this shows that there were statistically significant differences among the three groups regarding serum periostin (P<0.001).

In agreement with our result, Inoue et al. [12] found in their study that the serum periostin level was higher in the asthmatic group than in the control group [12].

There was insignificance correlation between age and BMI and serum periostin level (P=0.505 and 0.757, respectively), but there was highly significant correlation between FEV1%, FEV1/FVC%, PEF%, and eosinophil count and serum periostin level (P=0.002, 0.001, <0.001, and <0.001, respectively).

Song et al. [13] reported that there is a positive correlation of serum periostin and other biomarkers of type 2 immunity such as blood eosinophil count and FeNO in childhood and adult asthma. However, detected no correlations of blood eosinophil or FeNO with serum periostin in children with asthma.

In the study by Inoue et al. [12], periostin was slightly correlated with specific immunoglobulin E regarding to house-dust mite (P=0.035) and the eosinophil count (P=0.036), with no correlation of periostin with either %PEFR and %FEV1 or with %MMF except for those with PE.

From these results, we conclude that serum periostin increases in patients with asthma, and it is higher in atopic than nonatopic patient and can be consider as diagnostic biomarker of bronchial asthma. These finding are particularly useful for diagnosis of asthma and for developing therapeutic approach.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Horn BR, Robin ED, Theodore J, Van Kessel A. Total eosinophil counts in the management of bronchial asthma. N Engl J Med 1975; 292:1152–1155.  Back to cited text no. 1
    
2.
Takayama G, Arima K, Kanaji T. Periostin: a novel component of subepithelial fibrosis of bronchial asthma downstream of IL-4 and IL-13 signals. J Allergy Clin Immunol 2006; 118:98–104.  Back to cited text no. 2
    
3.
Lopez-Guisa JM, Powers C, File D. Airway epithelial cells from asthmatic children differentially express proremodeling factors. J Allergy Clin Immunol 2012; 129:990–997.  Back to cited text no. 3
    
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Jia G, Erickson RW, Choy DF. Periostin is a systemic biomarker of eosinophilic airway inflammation in asthmatic patients. J Allergy Clin Immunol 2012; 130:647–654.  Back to cited text no. 4
    
5.
Rosselli-Murai LK, Almeida LO, Zagni C. Periostin responds to mechanical stress and tension by activating the MTOR signaling pathway. PLoS One 2013; 8:e83580.  Back to cited text no. 5
    
6.
Gordon ED, Sidhu SS, Wang ZE. A protective role for periostin and TGF-b in IgE-mediated allergy and airway hyperresponsiveness. Clin Exp Allergy 2012; 42:144e55.  Back to cited text no. 6
    
7.
Bentley JK, Chen Q, Hong JY. Periostin is required for maximal airways inflammation and hyperresponsiveness in mice. J Allergy Clin Immunol 2014; 134:1433–1442.  Back to cited text no. 7
    
8.
Kanemitsu Y, Ito I, Niimi A. Osteopontin and periostin are associated with a 20-year decline of pulmonary function in patients with asthma. Am J Respir Crit Care Med 2014; 190:472e4.  Back to cited text no. 8
    
9.
Rasool R, Shera IA, Nissar S. Role of skin prick test in allergic disorders: a prospective study in Kashmiri population in light of review. Indian J Dermatol 2013; 58:1.  Back to cited text no. 9
    
10.
Sorkness RL, Bleecker ER, Busse WW. Lung function in adults with stable but severe asthma: air trapping and incomplete reversal of obstruction with bronchodilation. J Appl Physiol (1985) 2008; 104:394–403.  Back to cited text no. 10
    
11.
Horvath I, Hunt J, Barnes PJ. Exhaled breath condensate: methodological recommendations and unresolved questions. Eur Respir J 2006; 26:523–548.  Back to cited text no. 11
    
12.
Inoue T, Akashi K, Watanabe M. Periostin as a biomarker for the diagnosis of pediatric asthma. Pediatr Allergy Immunol 2016; 27:521–526.  Back to cited text no. 12
    
13.
Song JS, You JS, Jeong SI. Serum periostin levels correlate with airway hyper-responsiveness to methacholine and mannitol in children with asthma. Allergy 2015; 70: 674–681.  Back to cited text no. 13
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]
 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4]



 

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