scholarly journals Clinical parameters of inflammatory bowel disease in children do not correlate with four common polymorphisms of the transforming growth factor β1 gene.

2011 ◽  
Vol 58 (4) ◽  
Author(s):  
Anna Liberek ◽  
Joanna Jakóbkiewicz-Banecka ◽  
Anna Kloska ◽  
Joanna Świderska ◽  
Zbigniew Kmieć ◽  
...  

Transforming growth factor β1 (TGF-β1) is a cytokine affecting cell proliferation and development, which also has an immunomodulatory activity. Correlations between polymorphisms of the TGF-β1 gene and clinical parameters of inflammatory bowel disease (IBD) were reported previously in adults. Here, we tested whether such correlations occur in pediatric patients suffering from IBD. One hundred and four pediatric IBD patients were involved in this study. Among them, 36 were diagnosed with Crohn's Disease (CD) and 68 were diagnosed with ulcerative colitis (UC). The control group consisted of 103 children, in which IBD was excluded. TGF-β1 levels were determined in plasma and intestinal mucosa samples. The presence of the TGF β1 protein and the amount of TGF β1 mRNA were estimated in intestinal mucosa by immunohistochemistry and reverse transcription Real-Time PCR, respectively. Four common polymorphisms of the TGF-β1 gene were investigated: -800G/A, -509C/T, 869T/C and 915G/C. No significant correlation between TGF-β1 genotypes and (i) TGF-β1 levels in plasma and tissue samples, (ii) TGF-β1 gene expression efficiency in intestinal mucosa, (iii) IBD clinical parameters and (iv) inflammatory activity could be detected in children suffering from IBD. We conclude that, contrary to previous suggestions, the four common polymorphisms of the TGF-β1 gene do not influence the susceptibility to or clinical parameters of IBD in the tested population of children.

1970 ◽  
Vol 60 (4) ◽  
Author(s):  
Anna Liberek ◽  
Zbigniew Kmieć ◽  
Piotr M Wierzbicki ◽  
Joanna Jakóbkiewicz-Banecka ◽  
Tomasz Liberek ◽  
...  

Previously published studies on levels of the transforming growth factor-β1 (TGF-β1) protein and mRNA of the corresponding gene in patients suffering from inflammatory bowel diseases (IBD) gave varying results, leading to contradictory conclusions. To solve the contradictions, we aimed to assess longitudinally TGF-β1 protein and mRNA levels at different stages of the disease in children suffering from IBD. The study group consisted of 19 pediatric patients with IBD at the age between 3.5 and 18.4 years. The control group consisted of 42 children aged between 2.0 and 18.0 years. The plasma TGF-β1 concentration was measured with ELISA. mRNA levels of the TGF-β1 gene isolated from samples of the intestinal tissue were assessed by reverse transcription and real-time PCR. Levels of TGF-β1 protein in plasma and corresponding mRNA in intestinal tissue were significantly higher in IBD patients than in controls. TGF-β1 and corresponding transcripts were also more abundant in plasma and intestinal tissue, respectively, in patients at the active stage of the disease than during remission. In every single IBD patient, plasma TGF-β1 level and mRNA level in intestinal tissue was higher at the active stage of the disease than during remission. Levels of TGF-β1 and corresponding mRNA are elevated during the active stage of IBD but not during the remission. Longitudinal assessment of this cytokine in a single patient may help to monitor the clinical course of IBD.


Author(s):  
Rondius Solfaine ◽  
Lailatul Muniroh ◽  
Iwan Sahrial Hamid

Background: Coleus amboinicus extracts are known to have anti-oxidant activity, anti-platelet aggregations, antibacterial, anticancer and anti-inflammation. Objective: To evaluate Coleus amboinicus (CA) extracts in increasing of transforming growth factor-β1 concentration and molecular docking prediction of quercetin on receptor 4X0M (TGF-β1), measuring the levels of BUN, serum creatinine and Glutathione Peroxidase (GPx) on uric acid-induced rats. Method: Fourty-two male Wistar rats (Rattus norvegicus), 3 months, 150-200 g were allocated into 3 groups (n=14). The control group received placebo (U-0), treatment group were administered orally with uric acid 1,5% and oxonic acid 2% (U1) and received 500 mg/kg bw of the CA extracts (U-2) respectively for 30 days. Blood serums collected for analysis of creatinine and BUN concentrations. All groups were sacrificed to collect kidney for measuring of GPx activity and TGF-β1 concentration was conducted by avidin-horseradish peroxidase (HRP) sandwich-Elisa. Kidney organ was collected to histopathological analyzed by HE and PAS staining. Results: CA extract analyzed by TLC has a relative fraction of flavonoids, terpenes, saponins, polyphenols and alkaloids. Induction with uric acid has proven to causes acute renal failure with indicated of elevated BUN, serum creatinine concentration and necrotic lesions of tubular membrane in treatment groups. Treatment of CA extract at a dose of 500 mg/kg bw could increase of GPx and of TGF-β1 concentration significantly (p≤0.05). Quercetin as a marker compound of CA extract has stronger bind to the TGF-β1receptor (PDB code: 4X0M) than its of 3WA_601 ligand by in silico. Conclusion: CA extract is proven to inhibit acute renal failure by increasing of TGF-β1concentration and has strong binding of its receptor.


2011 ◽  
Vol 39 (4) ◽  
pp. 1061-1066 ◽  
Author(s):  
Thomas T. MacDonald ◽  
Iona Bell ◽  
Giovanni Monteleone

There are large numbers of T-cells in the mucosa of the intestine in healthy individuals. The stimulus for their presence is the normal gut microbiota. For unknown reasons, in patients with IBD (inflammatory bowel disease), there is inappropriate and chronic activation of mucosal T-cells which leads to gut damage and severe morbidity. In one form of IBD, namely Crohn's disease, the T-cells are probably responding to the microbiota. T-cell survival in the gut wall is dependent on pro-inflammatory cytokines and antibody-mediated inhibition of one of these cytokines, TNFα (tumour necrosis factor α), has shown efficacy in patients, thus encouraging investigations of other ways to control mucosal T-cell responses. In the present paper, we give a brief review of T-cell immunology in IBD and then discuss how two particular cytokines, namely IL-21 (interleukin 21), which is generally pro-inflammatory and important in gut T-cell survival and in maintaining Th17 cells, and TGFβ1 (transforming growth factor β1), which is generally immunosuppressive, play opposing roles in gut inflammation.


2020 ◽  
Vol 78 (2) ◽  
pp. 837-845
Author(s):  
Eman M. Khedr ◽  
Asmaa M.S. Gomaa ◽  
Omyma G. Ahmed ◽  
Hanaa M.M. Sayed ◽  
Ayman Gamea

Background: There are currently few biomarkers to assist in early diagnosis of dementias. Objective: To distinguish between different dementias: Alzheimer’s disease (AD), vascular dementia (VaD), and Parkinson’s disease dementia (PDD) using simple neurophysiologic (P300) and laboratory markers (transforming growth factor β1 “TGF-β1”). Methods: The study included 15 patients for each type of dementia and 25 age- and sex-matched control subjects. Dementia patients were diagnosed according to the Diagnostic and Statistical Manual of Mental Disorders 4th edition-revised (DSM-IV-R). Modified Mini-Mental State Examination (3MS), Memory Assessment Scale (MAS), P300, and TGF-β1 were examined for each participant. Results: There were no significant differences between groups as regard to age, sex, and education, social, and economic levels. Significant differences between groups were observed in registration and naming variables of the 3MS. Compared with the control group, P300 latency was prolonged in all groups, although to a greater extent in AD and PDD than in VaD. A serum level of TGF-β1 was significantly elevated in all groups but was significantly higher in AD and VaD than in PDD. 3MS tended to correlate with P300 more than TGF-β1, and to be stronger in AD than the other groups. Conclusion: Measurements of P300 latency and serum levels of TGF-β1 can help distinguish AD, PDD, and VaD. P300 was more prolonged in AD and PDD than VaD whereas TGF-β1 was significantly higher in AD and VaD than PDD. Thus P300 and TGF-β1 may be useful biomarkers for detection and evaluation of the extent of cognitive dysfunction.


2021 ◽  
Vol 2021 ◽  
pp. 1-6
Author(s):  
Shahram Bamdad ◽  
Fatemeh Sanie-Jahromi ◽  
Marzieh Alamolhoda ◽  
Nasrin Masihpour ◽  
Mohammad-Hossein Karimi

Background. To investigate the association of glutathione s-transferase omega 2 (GSTO2) (142N > D) and transforming growth factor-β1 (TGF-β1) (869T > C) gene polymorphisms on the pathogenesis of two common types of glaucoma (including primary open-angle glaucoma (POAG) and chronic angle-closure glaucoma (CACG)) in the Iranian population. Methods. A total of 100 glaucoma patients (60% males and 40% females with an age mean ± SD of 34.66 ± 14.25 years; 56 cases of POAG and 44 cases of CACG) were enrolled in this study. GSTO2 (142N > D) and TGF-β1 (869T > C) polymorphisms were evaluated by PCR-based methods in patients and controls. Results. At locus GSTO2 (142N > D), the odds of ND genotype with respect to DD and NN genotypes were 1.55 and 2.08 times higher in POAG and CACG patients compared to those of patients in the control group (95% CI1: 0.80–2.98; 95% CI2: 1.00–4.33) which was statistically significant in CACG patients. However, the odds of DD and NN genotypes against the reference genotype in two patients group were not statistically significant as compared to those of patients in the control group. There was a significant association between the ND genotype and male patients (OR = 2.28, 95% CI: 1.06–4.92). The analysis of TGF-β1 (869T > C) polymorphisms showed no significant difference between the genotypes of TGF-β1 (869T > C) polymorphisms in patients and control groups; however, the CT genotype of TGF-β1 significantly differed between female controls and patients (OR = 0.42, 95% CI: 0.18–0.96). Conclusion. The presented results revealed that there was a significant association between the ND genotype of GSTO2 and the pathogenesis of glaucoma. Furthermore, this genotype can be considered as a sex-dependent genetic risk factor for the development of glaucoma. In contrast, the CT genotype of TGF-β1 is suggested to be a protective genetic factor against the pathogenesis of glaucoma.


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