Browsing by Author "Mesquita, L"
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- Asthma and rhinitis have different genetic profiles for IL13, IL17A and GSTP1 polymorphismsPublication . Resende, EP; Todo-Bom, A; Loureiro, C; Mota-Pinto, A; Oliveiros, B; Mesquita, L; Silva, HCBACKGROUND: Asthma and rhinitis have a complex etiology, depending on multiple genetic and environmental risk factors. An increasing number of susceptibility genes are currently being identified, but the majority of reported associations have not been consistently replicated across populations of different genetic backgrounds. PURPOSE: To evaluate whether polymorphisms of IL4R (rs1805015), IL13 (rs20541), IL17A (rs2275913) and GSTP1 (rs1695) genes are associated with rhinitis and/or asthma in adults of Portuguese ancestry. METHODS: 192 unrelated healthy individuals and 232 patients, 83 with rhinitis and 149 with asthma, were studied. All polymorphisms were detected by real time polymerase chain reaction (PCR) using TaqMan assays. RESULTS: Comparing to controls, significant association with asthma was observed for GSTP1 rs1695 AA genotype (odds ratio (OR) - 1.96; 95% CI - 1.18 to 3.25; p=0.010). The association sustains for allergic asthma (OR - 2.17; 95% CI - 1.23 to 3.80; p=0.007). IL13 rs20541 GG genotype was associated with less susceptibility to asthma (OR - 0.55, 95% CI - 0.33 to 0.94, p=0.028). Among patients, IL17A rs2275913 AA genotype was less associated with asthma than with rhinitis (OR - 0.20; 95% CI of 0.07 to 0.56; p=0.002). A similar association was found for IL13 rs20541 GG genotype (OR - 0.48; 95% CI of 0.25 to 0.93; p=0.031). There were no significant differences in the distribution of allelic and genotypic frequencies between patients and controls for the IL4R polymorphism' analyzed. CONCLUSION: These results support the existence of a significant association between GSTP1 rs1695 and IL13 rs20541 SNPs, with susceptibility to asthma, in the population studied. Different genotype profiles of IL17A and IL13 genes seem to influence the clinical pattern of disease expression mainly confined to the upper airways, as rhinitis, or including the lower airways, as asthma.
- CD26/DPPIV and response to hepatitis B vaccinationPublication . Dourado, M; Alves, V; Mesquita, L; Ramos, I; Pinto, AM; Rosa, MSThe prevention of hepatitis B is important, since it is responsible for significant morbidity and mortality around the world. Unfortunately, hepatitis B vaccine does not always induce protective immunity. The lack of immune response to vaccine (non-responders) can depend on individual characteristics. The objective of this study was to correlate the CD26/DPPIV cellular expression and DPPIV serum activity with HBV vaccine response and its possible role as an indicator of immune competence acquisition. We also determined the cellular expression of CD3, CD19, CD56 and CD25 in peripheral blood T lymphocytes. Blood samples were obtained from 28 healthy human volunteers who were enrolled with a vaccination program. There were "responders" (RM = 13) and "non-responders" (NRM = 15), after vaccination. The lymphocyte populations were identified by flow cytometry. DPPIV serum activity was measured fluorimetrically. CD26 expression in responders (55.9 +/- 7.7%) versus in non-responders (51.9 +/- 7.0%) did not show a significant difference. The DPPIV serum activity in responders compared to in non-responder subgroup (59.9 +/- 8.4/50.3 +/- 10.6U/L) showed, however, a significant difference (P < 0.05). The expression of CD3, CD19 and CD56 on peripheral lymphocytes was similar between responders and non-responders. The expression of CD3CD26 (52.2 +/- 8.6%) and CD3CD25 (10.9 +/- 3.8%) in responders versus the expression of CD3CD26 (48.0 +/- 5.7%) and CD3CD25 (8 +/- 4.6%) in non-responders did not show statistically significant difference. CD25 referred as a marker of T lymphocyte activation was increased in responders (15.8 +/- 4.5%) versus in non-responders (10.1 +/- 4.8%), showing a significant difference (P = 0.003). It was, however, impossible to demonstrate an increase in CD3CD25 and CD3CD26 in the responder subgroup. This suggests that different lymphocyte subsets other than T cells are implicated in the response to hepatitis B vaccination.
- Doseamento das granzimas A e B na sarcoidose pulmonar (estudo experimental)Publication . Dourado, M; Bento, J; Mesquita, L; Marques, A; Vale-Pereira, S; Ribeiro, AB; Mota-Pinto, ASarcoidosis is a systemic disease of unknown aetiology, morphologically characterized by well-formed epithelioid granulomas, which show little or no central necrosis. These may be present in any organ or tissue. The lung is the most frequently and prominently involved target. The granuloma is often very sharply demarcated from the adjacent tissue and is surrounded by a mantle of lymphocytes, which mediate lysis of target cells by various mechanisms, including exocytosis of lytic proteins, perforins and granzymes. Sarcoidosis laboratorial diagnosis is usually made by SACE and Lisozyme dosages. The granzymes A and B could be two other markers of the disease, since the sarcoidosis granuloma is rich in cytotoxic and NK cells. An ELISA Kit was used to measure Granzyme A and B in serum of a normal control group (NC) (n=30), and in two groups with lung pathology: one without sarcoidosis, disease control (DC) (n=21) and other with sarcoidosis (S) (n=11). Our results showed that SACE activity is significantly augmented in S group comparing with NC and DC, respectively: 82,6+/-32,7/31,9+/-17,8 - p=0,00017 and 82,6+/-32,7/31,9+/-17,8 - p=0,00024. Lisozyme activity is significantly augmented in S and DC groups comparing with NC. Granzyme B showed a significant decrease in DC and S groups comparing with NC. Granzyme A showed a significant decrease between S/NC groups. Our results suggest that the decrease of Granzyme A and B in sarcoidotic patients could be related to an ineffective inflammatory local response related to the formation of sarcoidosis granulomas. More studies are needed, particularly in BAL.
- Envolvimento pulmonar subclínico em sarcoidose cutâneaPublication . Robalo-Cordeiro, C; Gonçalo, Margarida; Lima, MA; Mesquita, L; Teixeira, L; Santos-Rosa, M; Azevedo-Bernarda, R; Poiares-Baptista, A; Robalo-Codeiro, AJ