Percorrer por autor "Silva, Berta M."
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- Brain expression of inflammatory mediators in Mesial Temporal Lobe Epilepsy patientsPublication . Leal, Bárbara; Chaves, João; Carvalho, Cláudia; Rangel, Rui; Santos, Agostinho; Bettencourt, Andreia; Lopes, João; Ramalheira, João; Silva, Berta M.; da Silva, António Martins; Costa, Paulo P.Neuroinflammation may be central in epileptogenesis. In this study we analysed inflammatory reaction markers in brain tissue of Mesial Temporal Lobe Epilepsy with Hippocampal Sclerosis (MTLE-HS) patients. TLR4, IL-1β and IL-10 gene expression as well as the presence of activated HLA-DR+ microglia was evaluated in 23 patients and 10 cadaveric controls. Inflammation characterized by the presence of HLA-DR+microglia and TLR4, IL-1β overexpression was evident in hippocampus and anterior temporal cortex of MTLE-HS patients. Anti-inflammatory IL-10 was also overexpressed in MTLE-HS patients. Our results show that hippocampal neuroinflammation extends beyond lesional limits, as far as the anterior temporal cortex.
- Expression of Inflammation-Associated MicroRNAs in EpilepsyPublication . Leal, Bárbara; Carvalho, Cláudia; Chaves, João; Bettencourt, Andreia; Freitas, Joel; Lopes, João; Ramalheira, João; Silva, António M.; Costa, Paulo P.; Silva, Berta M.Background: Neuroinflammation appears as an important epileptogenic mechanism. MicroRNAs (miRNA) are small non-coding RNA molecules that function as post-transcriptional regulators of gene expression, controlling different biological process including immune system homeostasis and function. Evidences, both in patients and animal studies, have demonstrated an abnormal brain expression of miR-146a and miR-155 in Mesial Temporal Lobe Epilepsy (MTLE), the most refractory epilepsy type. Knowing that miR expression is very stable in biological fluids such as plasma or serum our aim was to characterize miR-146a and miR-155 expression in serum of MTLE and GGE patients. Methods: Expression levels of miR146a and RNU48 (reference gene) were quantified by Real-Time PCR in serum of 16 MTLE patients all with Hippocampal Sclerosis (6F, 8M, mean age= 44.1±11.7 years, age of onset= 13.5±10.6 years, 7 with Febrile Seizures antecedents). A group of 24 healthy individuals was used as control. Relative expression values were calculated using the 2-ΔΔCt method. Results: MTLE patients had a higher expression of miR-146a (6 fold) and miR-155 (2 fold) when compared to controls. Conclusion: Our results, although preliminary, show that miR-146a and miR-155 may be suitable biomarkers for epileptogenesis. It is thought that these miRNAs have role in fine-tuning the response to pro-inflammatory cytokines during epileptogenesis. Nevertheless its importance in epilepsy development it is yet not fully understood. The comprehension of this role may be relevant for the development of new therapeutic strategies.
- Vitamin D supplementation effects on FoxP3 expression in T cells and FoxP3+/IL-17A ratio and clinical course in systemic lupus erythematosus patients: a study in a Portuguese cohortPublication . Marinho, António; Carvalho, Cláudia; Boleixa, Daniela; Bettencourt, Andreia; Leal, Bárbara; Guimarães, Judite; Neves, Esmeralda; Oliveira, José Carlos; Almeida, Isabel; Farinha, Fátima; Costa, Paulo P.; Vasconcelos, Carlos; Silva, Berta M.Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with multi-organ inflammation, linked to loss of immune tolerance to self-antigens and the production of a diversity of autoantibodies, with a negative impact on the patients' quality of life. Regulatory T cells have been reported as deficient in number and function in SLE patients. However, some authors also described an enrichment of this cell type. The hypothesis that certain forms of autoimmunity may result from a conversion of Treg cells into a Th17 cell phenotype has been suggested by some studies. In fact, in SLE patients' sera, the IL-17 levels were observed as abnormally high when compared with healthy individuals. Environmental factors, such as vitamin D, that is considered a potential anti-inflammatory agent, combined with genetic and hormonal characteristics have been associated with SLE phenotype and with disease progression. The aim of this study was to evaluate the effect of vitamin D supplementation on FoxP3 expression and IL-17A-producing T cells, through FoxP3+/IL-17A ratio. Additionally, disease evolution, serum vitamin D levels, serum autoantibodies levels and calcium metabolism (to assure safety) were also studied. We assessed 24 phenotypically well-characterized SLE patients. All patients were screened before vitamin D supplementation and 3 and 6 months after the beginning of this treatment. Peripheral blood lymphocyte's subsets were analysed by flow cytometry. Serum 25(OH)D levels significantly increased under vitamin D supplementation (p = 0.001). The FoxP3+/IL-17A ratio in SLE patients after 6 months of vitamin D supplementation was higher than that in the baseline (p < 0.001). In conclusion, this study demonstrated that vitamin D supplementation provided favourable, immunological and clinical impact on SLE.