Abstract

Jundishapur J Nat Pharm Prod. 2021 August; 16(3):e100824.Published online 2021 July 17.doi: 10.5812/jjnpp.100824.Research ArticleGinger Extract Modulates the Production of Chemokines CCL17,CCL20, CCL22, and CXCL10 and the Gene Expression of Their Receptorsin Peripheral Blood Mononuclear Cells from Peptic Ulcer PatientsInfected withHelicobacter pyloriShila Jalalpour1, Vahid Mirzaee2, Mohammad Taheri3, Mahmood Sheikh Fathollahi4, HosseinKhorramdelazad1and Abdollah Jafarzadeh1, 5, *1Molecular Medicine Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran2Department of Internal Medicine, Rafsanjan University of Medical Sciences, Rafsanjan, Iran3Department of Microbiology, School of Medicine, Hamadan University of Medical Sciences, Hamadan, Iran4Assistant Professor of Biostatistics, Rajaie Cardiovascular Medical and Research Center, Iran University of Medical Sciences, Tehran, Iran5Department of Immunology, School of Medicine, Kerman University of Medical Sciences, Kerman, Iran*Corresponding author: Molecular Medicine Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran. Email:jafarzadeh14@yahoo.comReceived2020 January 18;Revised2020 October 14;Accepted2020 October 14.AbstractBackground:The imbalanced expression of chemokines plays critical role in the development ofHelicobacter pylori-mediated com-plications.Objectives:Our aim was to determine ginger extract (GE) effects on the expression of chemokines CCL17, CCL20, CCL22, and CXCL10,as well as CCR4, CCR6, and CXCR3 receptors by peripheral blood mononuclear cells (PBMCs) fromH. pylori-infected patients withpeptic ulcer (PU).Methods:Peripheral blood mononuclear cells were obtained from 20 patients withH. pylori-associated PU, 20H. pylori-infectedasymptomatic subjects (HAS), and 20 non-infected healthy subjects (NHS). The PBMCs were stimulated by 10μg/mL ofH. pylori-derived crude extract (HPCE) in the presence of 0, 10, 20, and 30μg/mL of GE. After 36 hours, the supernatant and the RNA extractedfrom the cells were tested for chemokine concentration and chemokine receptor expression using ELISA and real-time PCR tech-niques, respectively.Results:In PU patients, treating HPCE-stimulated PBMCs with 10, 20, or 30μg/mL GE reduced the production of CXCL10 (1.47, 1.5, and1.53 folds, respectively, P < 0.001 for all), CCL20 (1.44, 1.62, and 1.65 folds, respectively, P < 0.003), and treatment with 30μg/mL GEincreased CCL17 (1.28-fold, P < 0.001) and CCL22 (1.59-fold, P < 0.001) production compared with untreated HPCE-stimulated PBMCs.In PU patients, the HPCE-stimulated PBMCs treated with 10, 20, or 30μg/mL GE expressed lower levels of CXCR3 (1.9, 3, and 3.5 folds,respectively, P < 0.001) and CCR6 (2.3, 2.7, and 2.8 folds, respectively, P < 0.002) while treating with 10μg/mL GE upregulated CCR4(1.7 fold, P = 0.003) compared with untreated HPCE-stimulated PBMCs.Conclusions:Ginger extract modulated the expression of chemokines and their receptors in the PBMCs derived fromH. pylori-infected PU patients. The therapeutic potentials of ginger for treatingHP-related complications need to be further explored.