Yolanda Cataño Cañizalez; Edith Uresti Rivera; Rocio Garcia Jacobo; Diana Portales Perez; Yadira Bastian; J Rodriguez Rivera; Roberto Gonzalez Amaro; Jose Enciso Moreno; Mariana Garcia Hernandez
Abstract
Background: Chronic inflammation has critical role in Type 2 diabetes (T2D), in which IL-1β contributes in insulin resistance and beta cell dysfunction. The activation of NLRP3 and AIM2 by endogens ligands, such as mtDNA can lead to the release of active form of IL-1β. Objective: To evaluate ...
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Background: Chronic inflammation has critical role in Type 2 diabetes (T2D), in which IL-1β contributes in insulin resistance and beta cell dysfunction. The activation of NLRP3 and AIM2 by endogens ligands, such as mtDNA can lead to the release of active form of IL-1β. Objective: To evaluate AIM2 expression and activation as well as circulating mtDNA levels in T2D patients. Methods: AIM2 expression was analyzed by flow cytometry, it’s activity was assessed by measuring in vitro release of IL-1β induced by Poly (dA:dT), and mtDNA copy number was determined by quantitative real-time polymerase chain reaction. Results: Increased percent of AIM2+ cells were detected in monocytes from patients with T2D. Moreover, increased levels of IL-1β in monocytes cultures from T2D patients compared to healthy controls were observed. Also, association between AIM2+ cells and hyperglycemia (r=0.4385, P=0.0095) and triglycerides levels (r=0.5112, P=0.002) and waist-hip ratio (r=0.4710, P=0.0049) were detected. Likewise, the mtDNA copy number was augmented in T2D patients compared to control group. The mtDNA copies number was associated with body mass index (r=0.4231, P=0.0008) and TNF-α levels (r=0.5231, P=0.0005). In addition, increased levels of IL-12p70, TNF-a, IL-10, IL-6, IL-8 and IL-1β were detected in a serum from T2D patients. Conclusion: These results suggest the involvement of AIM2 and mtDNA in the inflammatory process seen in T2D.
Mandana Sattari; Alireza Fathiyeh; Fatemeh Gholami; Hassan Darbandi Tamijani; Mahdi Ghatreh Samani
Volume 8, Issue 1 , March 2011, , Pages 20-26
Abstract
Background: Growth factors play a major part in wound healing in many tissues including the periodontium. Transforming growth factor-β1 (TGF-β1) is one of these factors present in the gingival crevicular fluid. In addition, it is considered as one of the most important anti-inflammatory cytokines. ...
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Background: Growth factors play a major part in wound healing in many tissues including the periodontium. Transforming growth factor-β1 (TGF-β1) is one of these factors present in the gingival crevicular fluid. In addition, it is considered as one of the most important anti-inflammatory cytokines. Interleukin-1β is a proinflammatory cytokine that presents itself in gingival inflammation and the GCF. Such factors might be of value as prognostic markers of wound healing activity and the therapeutic progress following flap surgery. Objective: The aim of this study was to evaluate the effect of surgical flap on the concentration of IL-1β and TGF-β in the GCF of patients with moderate to severe chronic periodontitis. Methods: The GCF samples were collected, using the Perio-Paper strip at phase 1 (pre-surgery), phase 2 (4th week post surgery) and phase 3 (12th week post surgery) from 20 sites of 10 patients undergoing flap surgery. After the elution, IL-1β and TGF-β concentrations were measured by enzyme-linked immunosorbent assay (ELISA). Results: The mean TGF-β and IL-1β concentration decreased from phase 1 to phase 3 (p<0.05). There were no significant statistical correlations between IL-1β and TGF-β1 concentrations in the 3 assessment phases. There was a significant statistical correlation between TGF-β1 concentrations and the Plaque Index (PI) in phase 2 (p<0.05). There was a significant statistical correlation (p<0.05) between IL-1β and TGF-β1 concentration and the probing pocket depth (PPD). Conclusion: The flap surgery has a significant effect on decreasing IL-1β concentration. In the case of TGF-β1, probably the decrease in the concentration after treatment might be due to the removal of the inflammatory stimulants.
Shohreh Farshad; Manoochehr Rasouli; Akram Jamshidzadeh; Ayda Hosseinkhani; Aziz Japoni; Abdolvahab Alborzi; Alireza Taghavi; Hossein Kazemi Asl; Reza Ranjbar
Volume 7, Issue 2 , June 2010, , Pages 96-108
Abstract
Background: Previous studies imply that IL-1 and IL-8 gene variations may play a crucial role in the genetic predisposition to different gastric disorders upon H. pylori infection. Objective: The aim of this study was to determine the potential association between the prevalence of certain polymorphic ...
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Background: Previous studies imply that IL-1 and IL-8 gene variations may play a crucial role in the genetic predisposition to different gastric disorders upon H. pylori infection. Objective: The aim of this study was to determine the potential association between the prevalence of certain polymorphic sites and the risk of gastric disorders in Iranian population. Methods: One hundred and forty three unrelated individuals with different gastric disorders and 374 normal individuals with no gastric disorders and with a negative serology test for H. pylori (control group) were studied for the association between IL-1β (+3953 C/T) and IL-8 (-251 A/T) gene polymorphisms and H. pylorimediated gastritis and gastric ulcer. An analysis of genotype frequency for these genes was performed using RFLP-PCR. Results: Based on the data obtained from culture and pathologic findings, the patients were classified into three subpopulations: H pylori+ non-ulcerative gastritis+, H. pylori+ ulcerative gastritis+ and H. pylori- non-ulcerative gastritis+. A significantly higher frequency of TT genotype (p=0.02) in IL-1β +3953 in H. pylori+ ulcerative gastritis+ was revealed compared to the control group. There were no significant differences among other subpopulations. No significant differences in allele and genotype frequencies of IL-8 (-251A/T) were found among the patients. Conclusion: The data suggest that TT genotype in IL-1β +3953 may be a major contributing genetic risk factor for H. pylori induced gastric ulcer. Moreover, the role of other bacterial and host response factors, such as bacterial adherence peptides, host chemokines, and genes involved in gastric acid secretion, must be further investigated in different ethnic populations.
Kazem Ahmadi; Majid Riazipour
Volume 5, Issue 3 , September 2008, , Pages 177-180
Abstract
Background: T-2 toxin is a mycotoxin of type A trichothecenes produced by several fungal genera such as Fusarium species. Mycotoxins can affect both cell mediated and humoral immune compartments. Objective: The purpose of this study was to investi-gate the effect of T-2 toxin on cytokine production by ...
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Background: T-2 toxin is a mycotoxin of type A trichothecenes produced by several fungal genera such as Fusarium species. Mycotoxins can affect both cell mediated and humoral immune compartments. Objective: The purpose of this study was to investi-gate the effect of T-2 toxin on cytokine production by mouse peritoneal macrophages and lymph node T cells. Methods: Mouse peritoneal macrophages and lymph node T cells were isolated and treated with different concentrations of T-2 toxin and incubated at 370C and 5% CO2 in air for 48 hours. Cell free media were removed and used for cy-tokine assay by an ELISA method. Results: T-2 toxin significantly reduced IL-1β re-lease in a concentration dependent manner (p<0.005, p<0.001). Interleukin-12 and TNF-α production were significantly increased in response to 0.001ng/ml, 0.01ng/ml and 0.1ng/ml of T-2 toxin (p<0.001). However, T-2 toxin at higher concentrations rang-ing from 1ng/ml to 100ng/ml, reduced both IL-12 (p<0.001) and TNF-α production (p<0.005, p<0.05). The effects of T-2 toxin on lymph node T cells showed that IL-4 and IL-10 release was decreased in a concentration dependent manner (all with p<0.01). T-2 toxin at concentrations between 1ng/ml and 100ng/ml reduced the release of both IL-2 and IFN-γ (p<0.05, p<0.001). Conclusion: The results suggest that T-2 toxin at low concentrations can highly induce secretion of IL-12, TNF-α, IFN-γ and IL-2 and it may be used as a positive immunomodulator in the human model.