Melatonin has been proposed as regulating the immune system by affecting cytokine production in immunocompetent cells, enhancing the production of several T helper (Th)1 cytokines. To further investigate the melatonin's role in IL-2/IL-2R system, we established an inducible T-REx expression system in Jurkat cells in which the protein levels of HIOMT enzyme or MT(1) receptor were significantly down-regulated upon tetracycline incubation. We found that T-REx Jurkat cells with lower levels of HIOMT activity, and consequently lower content of endogenous melatonin, showed IL-2 production decrease after activation with lectin. Likewise, tetracycline-inducible stable cell line expressing MT(1) antisense produced decreased amounts of IL-2 (mRNA and protein levels) after stimulation. Moreover, in T-Rex-MT(1) cells incubated with tetracycline, a sub-optimal PHA dose failed to induce the early activation marker CD25 on the cell surface. The results shown here support the relevance of endogenous melatonin and its signaling in T cell activation.
These data support the relationships among periodontal disease and some biochemical parameters such as lipid and glucose data in pregnancy, and also among metabolic syndrome and biochemical parameters.
Background: Physiological changes during pregnancy, such as dilutional anemia and a reduced half-life of red blood cells, have prevented the use of glycated Hb (HbA1c) as a biomarker for gestational diabetes mellitus (GDM). Nevertheless, increasing evidence supports the use of HbA1c in GDM diagnostic strategies.We studied HbA1c as a biomarker of GDM and its possible use as a screening test to avoid the use of the glucose challenge test (GCT).Methods: This case-control study involved 607 pregnant women between the 24th and 28th week of gestation. HbA1c level was determined, and GDM was diagnosed according to the National Diabetes Data Group criteria. The area under the ROC curve (AUC) was determined; two low and two high cut-off points were established to rule out GDM and classify high-risk pregnant women, respectively. For each cut-off, sensitivity (S), specificity (SP), and total number and percentage of GCTs avoided were determined. Results:The AUC for HbA1c diagnostic performance was 0.68 (95% confidence interval 0.57-0.79). Using 4.6% HbA1c (27 mmol/mol) as the lower cut-off (S = 100%), 14% of participants could avoid the GCT. Using 5.5% HbA1c (36 mmol/mol) as the upper cut-off (SP = 94.5%), 6% of participants would be considered at high risk.Conclusions: HbA1c can be used as a screening test prior to the GCT, thereby reducing the need for the GCT among pregnant women at a low risk of GDM.
The glucose concentrations in tubes F stored at room temperature up to 3 hours were significantly lower (p < 0.05) than those measured in tubes C stored under the same conditions. We observed that it is in the first minutes after extraction, while the samples are collected and aliquots done, that the glucose consumption occurs in tubes F, but not in tubes C. There is a need to change the preanalytical conditions to prevent any loss of glucose. This will enable more accurate diagnosis and management of diabetes mellitus.
We proposed that women with fasting glycemia ≤ 62 mg/dL, (S = 91.3%, NPV = 98.79% and LR- = 0.87) are in low risk of suffering gestational diabetes, which means that 10% of our population would not undergo the glucose challenge test.
Adipose tissue is no longer considered mere energy storage, but an important endocrine organ that produces many signals in a tightly regulated manner. Leptin is one of the most important hormones secreted by the adipocyte, with a variety of physiological roles related with the control of metabolism and energy homeostasis. One of these functions is the connection between nutritional status and immune competence. The adipocyte-derived hormone leptin has been shown to regulate the immune response both in normal as well as in pathological conditions. Leptin´s modulation of the immune system is exerted at the development, proliferation, anti-apoptotic, maturation, and activation levels. The role of leptin in regulating immune response has been assessed in vitro as well as in clinical studies. Both the innate and adaptative immune responses are regulated by leptin. Every cell type involved in immunity can be modulated by leptin. In fact, leptin receptors have been found in neutrophils, monocytes, and lymphocytes, as well as belonging to the family of class I cytokine receptors. Moreover, leptin activates similar signaling pathways to those engaged by other members of the family. The overall leptin action in the immune system is a proinflammatory effect, activating proinflammatory cells, promoting T-helper 1 responses, and mediating the production of the other proinflammatory cytokines, such as tumor necrosis factor-, interleukin (IL)-2, or IL-6. Leptin receptor is also upregulated by proinflammatory signals. It has been shown that conditions of reduced leptin production are associated with increased infection susceptibility. Conversely, immune-mediated disorders such as autoimmune diseases are associated with increased secretion of leptin and production of proinflammatory pathogenic cytokines. Thus, leptin is a mediator of the inflammatory response, and could have also a permissive role in the development of autoimmune diseases.
The main issue in the prevention of myocardial infarction (MI) is to reduce risk factors. Periodontal disease is related to cardiovascular disease and both share risk factors. The purpose of this study is to investigate whether periodontitis can be considered a risk factor for MI and common risk factors in a case–control study and in a prospective follow-up study in patients with MI. The test group (MIG) was made up of 144 males who had MI in the previous 48 h. The control group (CG) was composed of 138 males without MI. Both groups were subdivided according to the presence or absence of stage III and IV of periodontitis. General data; Mediterranean diet and physical activity screening; periodontal data; and biochemical, microbiological and cardiological parameters were recorded. ANOVA, Mann–Whitney U and Kruskal–Wallis statistical tests and binary logistic regression analysis were applied. No differences in anthropometric variables were observed between the four groups. The average weekly exercise hours have a higher value in CG without periodontitis. The number of leukocytes was higher in MIG, the number of monocytes was higher in CG and the number of teeth was lower in MIG with periodontitis. Adherence to the Mediterranean diet was higher in CG. Porphyromonas gingivalis and Tannerella forsythia were higher in CG with periodontitis and in MIG with and without periodontitis. At follow-up, the left ventricular ejection fraction (LVEF) data were better in the non-periodontitis group: 15 patients had Mayor Cardiovascular Adverse Events (MACE), 13 of them had periodontitis and 2 did not show periodontitis. Periodontitis, exercise, diet and smoking are risk factors related to MI. MACE presented in the ‘MI follow-up’ shows periodontitis, weight, exercise hours and dyslipidemia as risk factors. LVEF follow-up values are preserved in patients without periodontitis. Our data suggest that periodontitis can be considered a risk factor for MI and MACE in the studied population.
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