Interleukin-6 and tumor necrosis factor-alpha gene polymorphisms in chronic idiopathic urticaria

Tavakol, Marzieh; Amirzargar, Ali Akbar; Movahedi, Masoud; Aryan, Zahra; Bidoki, Alireza Zare; Gharagozlou, Mohammad; Aghamohammadi, Asghar; Nabavi, Mohammad; Behniafard, Nasrin; Heidari, Kazem; Soltani, Shahin; Rezaei, Nima

doi:10.1016/j.aller.2013.06.004

Cited by 20 publications

(22 citation statements)

References 27 publications

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“…The gene expression in the CIU samples and normal control samples in the microarray data were analyzed. Actually, TGF-β signaling pathway was previously demonstrated to be involved in CIU, [23][24][25] which further proved that THBS1 might play a key role in CIU. It was found that most of these DEGs were highly expressed in CIU samples.…”

Section: Resultsmentioning

confidence: 76%

“…24,25 Proinflammatory cytokines, induced by activating macrophages and monocytes, may stimulate T and B lymphocytes, natural killer cells, and neutrophils, thus elevating the biosynthesis of prostaglandins and acute-phase proteins. In addition, it was observed that miR-194 and si-THBS1 could reduce the degranulation rate, histamine release rate, and HDMECs permeability of CIU mast cells.…”

Section: Discussionmentioning

confidence: 99%

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MicroRNA‐194 reduces inflammatory response and human dermal microvascular endothelial cells permeability through suppression of TGF‐β/SMAD pathway by inhibiting THBS1 in chronic idiopathic urticaria

Yang

Liu

2019

J of Cellular Biochemistry

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Chronic idiopathic urticaria (CIU) is a polyetiological dermatologic disease. Reports have stated that some microRNAs (miRNAs) have their roles to play in inflammatory response. In this present study, we aim to investigate whether miR‐194 has an effect on attenuating inflammatory response and human dermal microvascular endothelial cells (HDMECs) permeability of CIU mast cells through TGF‐β/SMAD pathway by binding to thrombospondin 1 (THBS1). The Gene Expression Omnibus database was used to obtain the CIU‐related microarray data, and then the analysis of differentially expressed genes was conducted and the miRNA regulated by THBS1 was predicted. After transfection of different mimic, inhibitor, or small interfering RNA, the effect of miR‐194 on inflammatory reaction, mast cell degranulation, histamine release rate, HDMECs permeability, and the expression of THBS1, interferon γ (IFN‐γ), TGF‐β, Smad3, and interleukin 4 (IL‐4) were detected. THBS1 was verified to be the miR‐194 target. After transfected with overexpressed miR‐194 and si‐THBS1, the degranulation rate, histamine release rate, and HDMECs permeability were significantly reduced, while the expression of IFN‐γ was higher, and the expression of THBS1, TGF‐β, Smad3, IL‐4 was significantly lower, accompanied with alleviated inflammatory reaction. Our study provides evidence that miR‐194 negatively modulates THBS1 and inhibits the activation of TGF‐β/SMAD pathway, thereby alleviating the inflammatory response and HDMECs permeability of mast cells in CIU.

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Section: Resultsmentioning

confidence: 76%

Section: Discussionmentioning

confidence: 99%

MicroRNA‐194 reduces inflammatory response and human dermal microvascular endothelial cells permeability through suppression of TGF‐β/SMAD pathway by inhibiting THBS1 in chronic idiopathic urticaria

Yang

Liu

2019

J of Cellular Biochemistry

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“…Pro-inflammatory cytokine genes SNPs seem to have been associated with a number of diseases [18][19][20][21][22][23][24]. We have recently shown that there is a significant association between the presence of the +565A of IL-6, −590 C of IL-4, codon 10/CT (rs1982037) TGF-β and FS [25][26][27].…”

Section: Introductionmentioning

confidence: 99%

Single nucleotide polymorphisms of TNF-Α gene in febrile seizures

Zare-Shahabadi

Ashrafi

Shahrokhi

et al. 2015

Journal of the Neurological Sciences

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“…It has inhibitory effects on mast cells and also controls proinflammatory cytokine release or their function [29]. It is not yet understood what is the specific role of IL-10 in urticaria, and still remain unclear this increase/decrease in IL-10 is a consequence of onset of CSU or compensatory response [26, 28].…”

Section: Discussionmentioning

confidence: 99%

“…TGF-β has been demonstrated to have the ability to promote apoptosis of mast cells. Meanwhile, it can suppress the expression of both of the FcεRI and IgE on mast cell surface [29]. Furthermore, it interferes with mediator release from mast cells so it may play an important role in homeostasis of mast cells [30].…”

Section: Discussionmentioning

confidence: 99%

Amelioration of patients with chronic spontaneous urticaria in treatment with vitamin D supplement

et al. 2017

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BackgroundSpontaneous urticaria is a common allergic skin condition affecting 0.5–1% of individuals and may burden on health care expenditure or may be associated with remarkable morbidity.AimIn this study, we measured the effect of vitamin D supplementation in patients with a diagnosis of CSU. Furthermore, quality of life and cytokine changes were evaluated.MethodsThe clinical trial was conducted on 20 patients with idiopathic chronic urticaria. Vitamin D was administered orally for 8 weeks and disease activity was measured pre- and post-treatment using USS and DLQI. On the other hand expressions of IL-17, IL-10, Foxp3, and TGF-β by Real-time RT-PCR were assessed.ResultsUSS questionnaire showed that severity of idiopathic urticaria after the intervention, which compared with the first day reached a significant 55% reduction. The DLQI quality of life questionnaire 2 months after treatment showed 55% improvement. Along with the significant improvement of clinical symptoms, use of vitamin D increase FOXP3 gene expression and downregulation of IL-10, TGF-B, and FOXP3, IL-17, but these changes were not statistically significant.LimitationThese might happen due to lack of enrolled population in the investigation.ConclusionVitamin D can be used along with standard medical care and it’s a safe and cost-effective method for the treatment of chronic urticaria with deficiency of vitamin D.

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Interleukin-6 and tumor necrosis factor-alpha gene polymorphisms in chronic idiopathic urticaria

Abstract: Pro-inflammatory cytokine gene polymorphisms can affect susceptibility to CIU. TNF-α promoter polymorphisms as well as IL-6 gene polymorphisms are associated with CIU.

Cited by 20 publications

References 27 publications

MicroRNA‐194 reduces inflammatory response and human dermal microvascular endothelial cells permeability through suppression of TGF‐β/SMAD pathway by inhibiting THBS1 in chronic idiopathic urticaria

MicroRNA‐194 reduces inflammatory response and human dermal microvascular endothelial cells permeability through suppression of TGF‐β/SMAD pathway by inhibiting THBS1 in chronic idiopathic urticaria

Single nucleotide polymorphisms of TNF-Α gene in febrile seizures

Amelioration of patients with chronic spontaneous urticaria in treatment with vitamin D supplement

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