Volume 9, Issue 3 (Aug 2021)
Res Mol Med (RMM) 2021, 9(3): 155-162 |
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Jahangiri S, Lotfi R, Mortazavi S H, Gorgin karaji A, Rezaiemanesh A, Rashidpour H et al . Decreased Gene Expression of Lipoxin A4 Receptor May Contribute to Nonallergic Rhinitis Pathogenesis. Res Mol Med (RMM) 2021; 9 (3) :155-162
URL: http://rmm.mazums.ac.ir/article-1-428-en.html
URL: http://rmm.mazums.ac.ir/article-1-428-en.html
Decreased Gene Expression of Lipoxin A4 Receptor May Contribute to Nonallergic Rhinitis Pathogenesis
Samira Jahangiri1 
, Ramin Lotfi2 , Seyed Hamidreza Mortazavi3 , Ali Gorgin karaji4 , Alireza Rezaiemanesh4 , Hatam Rashidpour5 , Farhad Salari 6
, Ramin Lotfi2 , Seyed Hamidreza Mortazavi3 , Ali Gorgin karaji4 , Alireza Rezaiemanesh4 , Hatam Rashidpour5 , Farhad Salari 6
1- Student Research Committee, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran
2- Lung Diseases and Allergy Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran
3- Department of Pediatrics, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran
4- Department of Immunology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran
5- Department of Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
6- Department of Immunology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran ,f.salari@kums.ac.ir
2- Lung Diseases and Allergy Research Center, Research Institute for Health Development, Kurdistan University of Medical Sciences, Sanandaj, Iran
3- Department of Pediatrics, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran
4- Department of Immunology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran
5- Department of Biotechnology, School of Pharmacy, Mashhad University of Medical Sciences, Mashhad, Iran
6- Department of Immunology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran ,
Abstract: (1921 Views)
Background: Rhinitis is a prevalent chronic inflammatory illness of the nasal mucosa. Arachidonic acid-derived lipoxin A4 (LXA4) has long been recognized to exert crucial antiinflammatory and pro-resolving effects on inflammatory responses through a specific receptor named LXA4 receptor/formyl peptide receptor-2 (ALX/FPR2). This study aimed to determine the serum level of LXA4 and the relative mRNA expression level of FPR2 in peripheral blood cells of patients with rhinitis (allergic and nonallergic) compared to healthy individuals.
Materials And Methods: The study groups consisted of 37 patients with Allergic Rhinitis (AR), 16 patients with Nonallergic Rhinitis (NAR), and 20 sex- and age-matched healthy individuals. The measurement of LXA4 serum level was performed by the Enzyme-Linked Immunosorbent Assay (ELISA) technique, and the analysis of FPR2 mRNA expression level was performed by quantitative real-time PCR method.
Results: The serum concentrations of LXA4 decreased in AR and NAR patients compared to healthy controls; however, this difference was not statistically significant (P>0.05). Besides, the mRNA expression level of FPR2 in peripheral blood cells of patients with nonallergic rhinitis was significantly lower than that in allergic rhinitis (P<0.05).
Results: The serum concentrations of LXA4 decreased in AR and NAR patients compared to healthy controls; however, this difference was not statistically significant (P>0.05). Besides, the mRNA expression level of FPR2 in peripheral blood cells of patients with nonallergic rhinitis was significantly lower than that in allergic rhinitis (P<0.05).
Conclusion: Our results suggest that reduced gene expression of FPR2 may contribute to developing persistent and chronic nasal mucosa inflammation seen in NAR patients. Therefore, stable analogs of LXA4 and its receptor agonist may help develop new therapeutic approaches for rhinitis.
Keywords: Allergic rhinitis, Inflammation, Omega-6 fatty acid, Lipoxin A4, Formyl peptide receptor-2
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