Submitted by Automa??o e Estat?stica (sst@bczm.ufrn.br) on 2016-07-25T23:07:30Z No. of bitstreams: 1 PatriciaIngridMacedoDeCastro_DISSERT.pdf: 960843 bytes, checksum: 3369f0056a2e2ab1f071631a2015066a (MD5) / Approved for entry into archive by Arlan Eloi Leite Silva (eloihistoriador@yahoo.com.br) on 2016-08-04T20:48:06Z (GMT) No. of bitstreams: 1 PatriciaIngridMacedoDeCastro_DISSERT.pdf: 960843 bytes, checksum: 3369f0056a2e2ab1f071631a2015066a (MD5) / Made available in DSpace on 2016-08-04T20:48:06Z (GMT). No. of bitstreams: 1 PatriciaIngridMacedoDeCastro_DISSERT.pdf: 960843 bytes, checksum: 3369f0056a2e2ab1f071631a2015066a (MD5) Previous issue date: 2015-11-30 / A pr?-ecl?mpsia ? uma doen?a que afeta 3-8% das mulheres gr?vidas. Os fatores de risco para essa doen?a n?o s?o completamente compreendidos, mas incluem desregula??o da resposta imune oriundos de defeitos na placenta??o, fatores ambientais e gen?ticos. O presente estudo teve como objetivo investigar associa??o varia??o na quantidade de receptores de citocinas pr?-inflamat?rias (IL-1R, IL-6R e TNF-?R) estariam envolvidos com a pr?-ecl?mpsia. Receptores de citocinas (IL-1R2, TNF-?R1 e IL-6R) foram avaliados em c?lulas mononucleares das gr?vidas normotensas (controle n=11) e gr?vidas com pr?-ecl?mpsia (PE, n=24). Mulheres com pr?-eclampsia tinham peso mais elevado no in?cio da gravidez (p=0.0171). Foi observado uma diminui??o de mon?citos cl?ssicos, mas n?o de mon?citos intermedi?rios e n?o-cl?ssicos na pr?-ecl?mpsia. A frequ?ncia dos receptores de citocinas proinflamat?rias IL-1R2, TNF-?R IL-6R aderidos a membrana das subpopula??es de mon?citos (cl?ssicos, intermedi?rios e n?o cl?ssicos) e linf?citos (CD3+CD4+ e CD3+CD8+) estavam diminu?das em pacientes com pr?-ecl?mpsia, quando comparados com gr?vidas normais. A redu??o na quantidade de receptores de citocinas IL-1R2, TNF-?R1 e IL-6R em mon?ciots e linf?citos pode ser um fator mantenedor do estado inflamat?rio na pr?-eclampsia. / Preeclampsia is a disease specific of human pregnancy that affects 3-8% of pregnant women, and it is one of the three leading causes of maternal mortality and morbidity. The disease is characterized by hypertension and proteinuria after the 20th week of gestation. The risk factors for this disease are not completely understood but appear to include dysregulation of the immune response arising from defects in placentation, environmental and genetic factors. This study aimed to determine whether the variation in the amount of proinflammatory cytokine receptors IL-1R2, IL-6R and TNF-?R1 would be involved in preeclampsia. They were recruited women with preeclampsia (n=24) and women who evolved during pregnancy without changes in blood pressure (n=12) were recruited. Clinical and laboratory data were collected. The cytokine receptors (IL-1R2, TNF-?R1 and IL-6R) were assessed in mononuclear cells isolated from peripheral blood using flow cytometry (Control = 8; PE = 24). C-reactive protein (CRP) was determined by CRP ultrasensitive method (Control = 7; PE = 18) was performed using sera pregnant women. Women with preeclampsia had higher weight at the beginning of the pregnancy (p=0.0171) and lower gestational age at delivery (0.0008). Classical monocytes were decreased in preeclampsia but not intermediate or non-classical monocytes. The frequency of IL-1R2 pro inflammatory cytokine receptors is decreased in women with PE only in the subpopulation of non-classical monocytes (p = 0.0011). TNF-?R1 receptor and IL-6R, had a decreased frequency in the three subpopulations of monocyte (classic, intermediate and non-classical) when compared to women with normal pregnancy. An increase in IL-1R2 receptor in TCD4+ lymphocytes, but a decrease in TNF-receptor and IL-6R in women with preeclampsia were found. No differences in the frequency of those receptors in CD3+/CD8+ in preeclampsia. There was no difference in C-reactive protein in preeclampsia. The reduction in the amount of IL-1R2, TNF- ?R1 and IL-6R monocytes and lymphocytes can be involved in the regulation of inflammation observed in preeclampsia, contributing to disease.