Investigating the Relationship between FGF2 Gene Expression and Airway Remodeling in Severe Asthma

Mahsa Manafi Varkiani; Majid Mirsadraee; Mohammadreza Khakzad; Soheila Moadikhah; Simin Moadikhah; Amirhossein Hashemiattar

doi:10.18502/ijaai.v24i1.18015

Mahsa Manafi Varkiani Innovative Medical Research Center, Faculty of Medicine, Mashhad Medical Science, Islamic Azad University, Mashhad, Iran
Majid Mirsadraee Department of Internal Medicine, Faculty of Medicine, Mashhad Medical Science, Islamic Azad University, Mashhad, Iran
Mohammadreza Khakzad Innovative Medical Research Center, Faculty of Medicine, Mashhad Medical Science, Islamic Azad University, Mashhad, Iran
Soheila Moadikhah Innovative Medical Research Center, Faculty of Medicine, Mashhad Medical Science, Islamic Azad University, Mashhad, Iran
Simin Moadikhah Innovative Medical Research Center, Faculty of Medicine, Mashhad Medical Science, Islamic Azad University, Mashhad, Iran
Amirhossein Hashemiattar Department of Radiology, Mashhad Medical Sciences Branch, Islamic Azad University, Mashhad, Iran

DOI: https://doi.org/10.18502/ijaai.v24i1.18015

Keywords: Asthma; Airway remodeling; Fibroblast growth factor 2; High-resolution computed tomography

Abstract

Severe asthma causes chronic airway inflammation and structural changes in the bronchial wall. Fibroblast growth factor 2 (FGF2) plays an inflammatory role in specific pathways in airway remodeling in asthma. Assessing the relationship between sputum pattern, bronchial thickness by high-resolution computed tomography (HRCT) scan, and FGF2 expression level can evaluate the role of FGF2 in asthma remodeling.

The study aimed to investigate the correlation between airway wall thickness and FGF2 gene expression in 100 participants with severe asthma. The method involved measuring airway wall thickness using HRCT and analyzing FGF2 gene expression through real-time reverse transcriptase polymerase chain reaction. The participants were divided into 2 groups based on bronchodilator responsiveness and classified into different asthma phenotypes based on sputum cell count.

The baseline data did not show a significant difference between the groups. The study found significant differences in airway variables between different asthma subgroups. FGF2 expression was associated with various characteristics of asthma, including body mass index, forced expiratory volume in 1 second (FEV1), and airway wall thickness. The receiver operating characteristic curve analysis showed that a fold change higher than 2.42 in FGF2 expression indicated asthma.

Based on our research, FGF2 may play a critical role in airway thickness regardless of inflammation. We found increased FGF2 levels with disease severity and wall thickness in atopic severe persistent asthma patients with FEV1 below 60%. Further research is needed to understand FGF2's role across broader FEV1 ranges and other phenotypes.