Fatemeh Kamankesh; Ali Ganji; Ali Ghazavi; Ghasem Mosayebi
Abstract
Background: Experimental autoimmune encephalomyelitis (EAE), as an autoimmune disease in the central nervous system (CNS), is an animal model for multiple sclerosis (MS) mediated by T lymphocytes.Objective: To investigate ginger extract’s effect on reducing inflammation and improving the symptoms ...
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Background: Experimental autoimmune encephalomyelitis (EAE), as an autoimmune disease in the central nervous system (CNS), is an animal model for multiple sclerosis (MS) mediated by T lymphocytes.Objective: To investigate ginger extract’s effect on reducing inflammation and improving the symptoms in the EAE model.Methods: The EAE was induced by injecting MOG35-55 and pertussis toxin into eight-week-old female C57BL6 mice. The mice were treated with an intraperitoneal injection of 300 mg/kg/day of hydroalcoholic extract of ginger for 21 days. The disease severity and weight changes were measured daily. Then, the mice spleens were removed; the gene expressions of interleukin (IL)-17, transforming growth factor beta (TGF-β), interferon-γ (IFN-γ), and tumor necrosis factor α (TNF-α) were analyzed by Real-time PCR and the percentage of regulatory T lymphocytes (Treg cells) was determined by flow cytometry. Serum nitric oxide and antioxidant capacity were measured, and brain tissue sections were prepared to investigate the leukocyte infiltration and plaque formation.Results: The severity of symptoms in the intervention group was lower than in the control. The gene expression levels of inflammatory cytokines, including IL-17 (P=0.04) and IFN-γ (P=0.01), were reduced. The Treg cells increased significantly, and the serum nitric oxide level was lower in the ginger-treated group. There was no significant difference in lymphocyte infiltration in the brain between the two groups.Conclusion: The present study indicated that ginger extract could effectively reduce inflammatory mediators and modulate immune responses in EAE.
Ehsanollah Ghaznavi-Rad; Khadijeh Khosravi; Nader Zarinfar; Ghasem Mosayebi
Volume 14, Issue 3 , September 2017, , Pages 215-222
Abstract
Background: Brucella is a well-known intracellular bacterium entailing acute and chronic illnesses in humans and domestic animals. The infection chronicity may be affected by the cell-mediated immunity and cytokine patterns. Objective: To evaluate the patterns of T-helper cytokines in patients suffering ...
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Background: Brucella is a well-known intracellular bacterium entailing acute and chronic illnesses in humans and domestic animals. The infection chronicity may be affected by the cell-mediated immunity and cytokine patterns. Objective: To evaluate the patterns of T-helper cytokines in patients suffering from chronic and acute brucellosis. Methods: In this cross-sectional study, 22 individuals with acute brucellosis, 21 individuals with chronic brucellosis, and 21 healthy individuals with the same genetic background were recruited from October 2015 to April 2016. Peripheral lymphocytes were isolated and stimulated by phytohemagglutinin (PHA) and brucella antigen in cell culture. The lymphocyte proliferation was detected by MTT assay. After collecting the supernatants, and through the use of ELISA method, we quantified the interferon gamma (IFN-γ), interleukin (IL)-5, IL-17 and transforming growth factor–beta (TGF-β). Results: Patients with chronic brucellosis had a lower level antigen-specific stimulation index compared to those suffering from acute brucellosis (p=0.0001). Cases with chronic brucellosis had a lower level of IFN-γ compared to cases with acute brucellosis (p=0.001). Finally, patients with chronic brucellosis had higher levels of IL-5 and TGF-β in comparison with the acute group (p=0.01 and p=0.04, respectively).Conclusion: Chronic brucellosis reduces lymphocyte proliferation and TH1 cytokine secretion, but it enhances IL- 5 and TGF-β production. Polarizing the immune responses plays a crucial part in the progression and development of chronic diseases.