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Publication
Expressão génica de genes associados à morte celular por apoptose em LES
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Abstract(s)
Introdução: O Lúpus Eritematoso Sistémico (LES) é uma doença auto-imune
crónica sistémica com múltiplas alterações imunológicas e que apresenta uma
grande diversidade de manifestações clínicas. É caraterizada pela produção de
auto-anticorpos e pela infiltração de células inflamatórias nos tecidos alvo.
Os neutrófilos são células fagocíticas com um tempo de semi-vida curto,
sendo das primeiras células a serem recrutadas do sangue periférico para o local
de inflamação, contribuindo desta forma para o processo inflamatório.
Embora a etiopatogenia do LES não esteja completamente compreendida,
considera-se que as anormalidades do processo apoptótico possam estar
envolvidas no desenvolvimento da doença. Apoptose é também essencial para o
estabelecimento de tolerância imune.
Neste sentido fomos quantificar a expressão genética de Fas-L, Bcl-2,
TNFα e TNFR1 em neutrófilos do sangue periférico purificados de doentes com
LES activo, inactivo e de um grupo controlo, correlacionando estes dados com
parâmetros de atividade da doença.
O grupo de doentes com LES era constituído por 45 mulheres e 4 homens
com uma média de idades de 35,3±11,5 e 23,5±4,2 anos, respetivamente, o grupo
controlo era constituído por 30 indivíduos saudáveis com uma média de idades de
30±6 anos.
Métodos: Analisou-se a expressão do RNAm da Bcl-2, Fas-L, TNFR1 e TNFα
em neutrófilos do sangue periférico, separados por cell sorting. A quantificação da
expressão de mRNA foi efectuada através de PCR em tempo real.
Resultados: Verificou-se um aumento da expressão genética de TNFR1 em
doentes com a doença activa e de uma maneira geral, em LES, uma diminuição da
expressão de Bcl-2, de TNFα e de Fas-L.
Conclusão: Os resultados sugerem a presença de alterações na expressão genética
de genes associados à morte celular por apoptose, em neutrófilos do sangue
periférico de doentes com LES, o que pode contribuir para a neutropenia que
ocorre nesta doença.
Introduction: The Systemic Lupus Erythematosus (SLE) is a chronic systemic auto-immune disease with multiple immunologic abnormalities that presents a variety of clinical manifestations. It is characterized by the production of autoantibodies and the infiltration of inflammatory cells on target tissues. The neutrophils are phagocytes with short half-life, being the first to be recruited from the peripheral blood to the inflammation site, and therefore contributing to the inflammatory process. Even though the etiopathogeny of SLE is not fully understood, it is considered that abnormalities in the apoptosis process might be involved in the disease development. Apoptosis is also essential to the establishment of immune tolerance. Therefore our purpose was to quantify the genetic expression of Fas-L, Bcl-2, TNFα and TNFR1 in purified peripheral blood neutrophils from active SLE patients, inactive SLE patients, and from a control group, correlating the obtained results with activity parameters of the disease. The SLE patients group was composed by 45 women and 4 men with an average age of 35,3±11,5 e 23,5±4,2 years, and a control group formed by 30 healthy individuals with an average age of 30±6 years. Methods: We analyzed the mRNA expression of Bcl-2, Fas-L, TNFR1 and TNFα in peripheral blood purified neutrophils by real time PCR. Results: Our results suggest that patients with active SLE express higher amounts of TNFR1, and in general, we observed, in SLE patients, lower mRNA levels of Bcl-2, TNFα and Fas-L. Conclusion: Based in our results, we suggest that some modifications occurred in the mRNA expression of genes associated with apoptosis cell death in peripheral blood neutrophils from SLE patients,that can contribute, at least in part, to the neutropenia observed in the disease.
Introduction: The Systemic Lupus Erythematosus (SLE) is a chronic systemic auto-immune disease with multiple immunologic abnormalities that presents a variety of clinical manifestations. It is characterized by the production of autoantibodies and the infiltration of inflammatory cells on target tissues. The neutrophils are phagocytes with short half-life, being the first to be recruited from the peripheral blood to the inflammation site, and therefore contributing to the inflammatory process. Even though the etiopathogeny of SLE is not fully understood, it is considered that abnormalities in the apoptosis process might be involved in the disease development. Apoptosis is also essential to the establishment of immune tolerance. Therefore our purpose was to quantify the genetic expression of Fas-L, Bcl-2, TNFα and TNFR1 in purified peripheral blood neutrophils from active SLE patients, inactive SLE patients, and from a control group, correlating the obtained results with activity parameters of the disease. The SLE patients group was composed by 45 women and 4 men with an average age of 35,3±11,5 e 23,5±4,2 years, and a control group formed by 30 healthy individuals with an average age of 30±6 years. Methods: We analyzed the mRNA expression of Bcl-2, Fas-L, TNFR1 and TNFα in peripheral blood purified neutrophils by real time PCR. Results: Our results suggest that patients with active SLE express higher amounts of TNFR1, and in general, we observed, in SLE patients, lower mRNA levels of Bcl-2, TNFα and Fas-L. Conclusion: Based in our results, we suggest that some modifications occurred in the mRNA expression of genes associated with apoptosis cell death in peripheral blood neutrophils from SLE patients,that can contribute, at least in part, to the neutropenia observed in the disease.
Description
Keywords
Lúpus Eritematosos Sistémico Neutrófilos Fas-L Bcl-2 TNFα TNFR1 Systemic Lupus Erythematosus Neutrophils