Search

Vitamin 3 is known to have an effect on the immune function. We investigated the immunomodulatory capability of vitamin 3 in HIV-infected patients and studied the expression of chemokine receptors on regu-latory T cells (Treg). Vitamin 3-deficient HIV-l-seropositive subjects were treated with cholecalciferol (vitamin 3) at a dose of 800IU daily for 3 months (n = 9) or 25,000 IU weekly for 2 months (n = 7). Peripheral blood mononuclear cells (PBMCs) were isolated and analyzed for skin-homing (CCR4 and CCR10) and gut-homing (CCR9 and integrin α4/β7) marker expression on Treg, by flow cytometry, before and after supplementation. Serum 25(OH)3 and parathyroid hormone (PTH) levels were determined at baseline and after the treatment period. Weekly doses of 25,000 IU cholecalciferol effectively achieved the optimal target serum 25(OH)3 con-centration of >75nmol/liter (30ng/ml) in HIV-infected patients. High-dose cholecalciferol supplementation differentially influenced skin-homing markers on Treg with an increased level of CCR10 expression and while a reduction in CCR4 expression level was observed together with a lower percentage of Treg expressing CCR4. For both dosing regimens, there were no significant differences in the expression of gut-homing markers, CCR9, and integrin α4/β7. High-dose vitamin 3 supplementation is needed to reverse vitamin 3 deficiency in HIV-infected individuals and this results in modulation of skin-homing markers but not gut-homing markers ex-pression on Treg. At a standard dose of 800IU/day, vitamin 3 is not effective in achieving an optimal 25(OH)3 concentration in patients with an underlying T cell dysfunction and is unable to exert any immu-nomodulatory effects. [ABSTRACT FROM AUTHOR]

Summary Vitamin D3 is known to induce regulatory T (Treg) cells by rendering antigen-presenting cells tolerogenic, its direct effect on human naturally occurring Treg cells is unclear. Here, we investigated if and how 1,25-dihydroxyvitamin D3 [1,25(OH)2D3] can directly affect the proliferation and function of human naturally occurring Treg cells in vitro. First, we demonstrated that these Treg cells express vitamin D receptors that were up-regulated following anti-CD3/CD28-bead stimulation. 1,25(OH)2D3 inhibited proliferation of Treg cells even when exogenous interleukin-2 was provided. Treg cells were more susceptible to the inhibitory effect of 1,25(OH)2D3 than conventional T cells. 1,25(OH)2D3 neither affected the anergic state nor the suppressive function of Treg cells but induced a subtle increase in interleukin-10-secreting cells. The cell-division-inhibiting effect of 1,25(OH)2D3 on Treg cells was also demonstrated in vivo by supplementing vitamin D-deficient HIV-1-infected patients with 2000 IU cholecalciferol (vitamin D3). Increased serum 1,25(OH)2D3 levels were associated with a drop in the number and percentage of Treg cells, which may be attributed to a decrease in the proliferating Foxp3+ Treg cell population. In conclusion, 1,25(OH)2D3 directly affects Treg cell growth and promotes interleukin-10 production without apparent effects on activation status and suppressive phenotype whereas in vivo, high serum 1,25(OH)2D3 levels are associated with reduced Treg cell proliferation and a reduced number of Treg cells. [ABSTRACT FROM AUTHOR]

Objectives: Dengue fever may manifested without or with warning sign (DWOWS or DWS) and severe dengue (SD) (WHO 2009). DWOWS can be distinguished from DWS if there is plasma leakage that can be showed by changes in plasma (increased hematocrite) or detecting ascites or pleural effusion by USG. Standard abdominal ultra-sound examination (USG) could found plasma leakage, but this equipment is costly and impractical in daily use. In this study we examined the role of pocket USG device to detect plasma leakage as alternative to ordinary USG. Methodology: Dengue fever patients are included prospectively in HSH since March 2011 until March 2012, examined appropriately to confi rm and classify dengue disease. Pocket USG (P02742, 3.5 Mhz, Signos, Australia) was used to fi nd ascites, pleural efusion or thickened gallbladder wall (defi ned as wall thickness >0.35 cm). Examined bedside on hospitalized day 1, 3 and 5 for every patients. Analysis was conducted assessing contribution of this USG examination to detect of plasma leakage in comparison with increased hematocrite. Results: Sixty nine dengue patients were enrroled with characteritis as, fever median duration of 6-7 days, 31 male (45%) with a mean±SD age of 33±15 years. Hct increase (as indicator of plasma leakage) has detected in 22 (31.9 %) of the group. Pocket USG detected ascites in 12 (17.4%), pleural efusion 10 (14.5%). GBT in 22 (31.9%), and pericholecystic fl uid in 5 (7.2%) of the patients. Fluid accumulation mostly detect in median day of fever 6 (range 3-8) days. Overall, fl uid accumulation as plasma leakage was detected by USG in 27 (39.1%) where as hematocrite increased were found in 22 (31.9%) (p<0.05). GBT were compared to hematocrite for severe dengue (SD), (p<0.01, OR 64.50, 95% CI 9.54-436.20). In comparison with standard USG accuracy was reasonably well. Based on these, we can clasify dengue patient into 42 (60.9%) DWOWS, 22 (31.9%) DWS and 5 (7.2%) SD. Conclusion: Pocket USG allows detection of plasma leakage including GBT related to severity of dengue infection more sensitive than Hct. Because of its portability, it can be used bedside and in emergency room rapidly. [ABSTRACT FROM AUTHOR]