The repercussion on the immune response of the expression of intraspecific aggressiveness in the face of a stressor agent was investigated in rats. Ninety-day-old animals were divided into three groups: the control group (only immunological measurements were performed), the foot-shock (FS) (animals individually receiving FS), and the intraspecific aggressive response (IAR) group (animals receiving FS and presenting IAR). For immunological measurements, blood samples were collected promptly at 7 and 15 days after FS or IAR. The FS reduced the total leukocyte amount presented. However, aggressiveness triggered not only reduction of the leukocytes, but also lymphocyte decrease and neutrophil increase. Moreover, an elevation in total leukocytes associated with an increase in the humoral immune response was also observed one week after IAR. In this study, the expression of intraspecific aggressiveness in the face of a stressor seemed to activate the immune system and to potentiate the antigen specific humoral response.Key words: intraspecific aggressiveness, leukocytes, humoral immune response. RESUMOA expressão de uma reação agressiva intra-específica diante de um estressor altera a resposta imune em ratos A repercussão sobre a resposta imune da expressão da agressividade intra-específica diante de um estressor foi investigada em ratos. Aos 90 dias de vida, os animais foram divididos em três grupos: grupo-controle (foram realizadas apenas mensurações imunológicas), choque nas patas (FS) (os animais receberam FS individualmente) e grupo resposta agressiva intra-específica (IAR) (os animais receberam FS e apresentaram IAR). Para as medições imunológicas, amostras de sangue foram coletadas imediatamente, 7 e 15 dias após FS ou IAR. O FS reduziu a quantidade total de leucócitos. Contudo, a agressividade foi acompanhada, além da redução do número de leucócitos, por diminuição de linfócitos e aumento de neutrófilos. Além disso, também foi observada elevação no número de leucócitos associada a aumento na resposta imune humoral uma semana após as IAR. Neste estudo, a expressão da agressividade intra-específica diante de um estressor parece ativar o sistema imune e potencializar a resposta humoral antígeno específica.Palavras-chave: agressividade intra-específica, leucócitos, resposta imune humoral.

RESUMO Investigamos em portadores de esquistossomose hepatoesplênica após esplenectomia com ou sem auto-implante esplênico: índice de aderência, produção de superóxido (SP) e de TNF-α em monócitos, tratados ou não com tuftsina. Avaliamos três grupos: voluntários sadios CG (grupo controle) (n=12); esplenectomizados com auto-implante AG (n=18) e esplenectomizados sem auto-implante WAG (n=9

OBJETIVO: Investigar os níveis de produção de SOD por monócitos periféricos em pacientes jovens portadores de esquistossomose hepatoesplênica submetidos à esplenectomia, ligadura da veia gástrica esquerda e auto-implante de tecido esplênico. MÉTODO: Quatro grupos foram envolvidos na investigação: G1 - 12 portadores de esquistossomose hepatoesplênica (EHE) sem tratamento; G2 - 13 portadores de EHE que receberam tratamento clínico e se submeteram à operação para descompressão do sistema porta: esplenectomia e ligadura da veia gástrica esquerda (EHE/ELGE); G3 - 19 pacientes jovens similares a G2, mas que receberam também auto-implante de tecido esplênico no omento maior (EHE/ELGE/AI); e G4 - 15 indivíduos sem infecção pelo S. mansoni advindos da mesma área geográfica, apresentando as mesmas condições sócio-econômicas (GC). RESULTADOS: Os indivíduos normais (GC - sem esquistossomose) apresentam níveis de SOD significantemente menores que os portadores de EHE sem tratamento (p<0,01); e aqueles do grupo EHE/ELGE (p<0,05). Os níveis de SOD do grupo EHE/ELGE/AI são estatisticamente similares ao grupo GC (p>0,05). CONCLUSÃO: Os resultados corroboram a hipótese de que o tratamento clínico associado à esplenectomia, ligadura da veia gástrica esquerda e auto-implante de tecido esplênico, em portadores jovens de esquistossomose hepatoesplênica, tendem a manter a resposta imune desses indivíduos.

Nitric oxide monocyte production levels in patients with the hepatosplenic form of Scistosoma mansoni infection 4 -ORIGINAL ARTICLE Nitric oxide monocyte production levels in patients with the hepatosplenic form of Scistosoma mansoni infection who underwent splenectomy, ligature of the left gastric vein and auto implantation of spleen tissue in the major omentum 1 Níveis de óxido nítrico produzidos por monócitos em portadores de esquistossomose hepatoesplênica que se submeteram a esplenectomia, ligadura da veia gástrica esquerda e auto-implante de tecido esplênico no omento maior ABSTRACT Purpose:To measure the levels of NO production by monocytes in patients with the hepatosplenic form of schistosomiasis mansoni who underwent splenectomy, ligature of the left gastric vein and auto implantation of spleen tissue in the major omentum. Methods: Four groups of volunteers were enrolled in the investigation: G1 -12 patients with S. mansoni infection in its hepatosplenic form without any kind of treatment (SMH); G2 -13 SMH patients who underwent medical treatment and portal hypertension decompression -splenectomy and ligature of the left gastric vein (SMH/SLGV); G3 -19 patients similar to the later group, but additionally received auto implantation of spleen morsels in the major omentum (SMH/SLGV/AI); and G4 -15 individuals with no S. mansoni infection coming from the same geographical area and presenting similar socio economical status (CG). Nitrite production by monocytes was determined by a standard Griess reaction adapted to microplates. The results were presented by mean ± SD for each group. Significant differences in NO production by monocytes were determined by Tukey-Kramer multicomparisons test. Probability values of 0.05 were considered significant. Results: Patients from G1 (SMH) showed lower level of NO production by monocytes (5.28 ± 1.28µmol/ml). Patients from G2 (SMH/SLGV) showed similar results (6.67 ± 0.44µmol/ml -q = 2.681 p > 0.05). Individuals of G4 (CG) showed higher level of NO production by monocytes (8.19 ± 2.74µmol/ml). Patients from G3 (SMH/SGLV/AI) showed similar NO production by PBMC as compared to individuals of G4 (CG) -(7.41 ± 1.65µmol/ml -q = 1.615 p > 0.05). The volunteers from G4 (CG) and G3 (SMH/SLGV/AI) showed significantly greater levels of NO production by monocytes as compared to those from G1 (SMH) -(q = 5.837 p < 0.01, and q = 4.285 p < 0.05). Conclusion: Collectively, the results point to a restoration of NO normal production by monocytes in SHM patients who underwent medical and surgical treatments, especially in those who had received auto implantation of spleen tissue in the major omentum after splenectomy and ligature of the left gastric vein. The data gives further support to the hypothesis that this additional procedure is important in the restoration of the immune response of these patients, since NO synthesis by the monocytes correlates with protective immunity against infection; thus, protecting them against overwhelming post splenectomy infection. Key words: Schistoso...

Cerebral palsy (CP) is characterized by motor disorders, including deficits in locomotor activity, coordination, and balance. Selective serotonin reuptake inhibitors have been shown to play an important role in brain plasticity. This study investigates the effect of neonatal treatment using fluoxetine on locomotor activity and histomorphometric parameters of the primary somatosensory cortex (S1) in rats submitted to an experimental model of CP. CP was found to reduce bodyweight and locomotion parameters and also to increase the glia/neuron index in the S1. Administration of fluoxetine 10 mg/kg reduced bodyweight, impaired locomotor activity parameters, and increased the number of glial cells and the glia/neuron ratio in the S1 in rats with CP. However, treatment with fluoxetine 5 mg/kg was not found to be associated with adverse effects on locomotor activity and seems to improve histomorphometric parameters by way of minor changes in the S1 in animals with CP. These results thus indicate that experimental CP, in combination with the use of a high dose of fluoxetine (10 mg/kg), impairs locomotor and histomorphometric parameters in the S1, while treatment with a low dose of fluoxetine (5 mg/kg) averts the negative outcomes associated with a high dose of fluoxetine in relation to these parameters but produces no protective effect.