10
views
0
recommends
+1 Recommend
1 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Efeito do estresse pré-natal na regulação da inflamação alérgica pulmonar no modelo murino de asma experimental Translated title: Effect of prenatal stress in regulating pulmonary allergic inflammation in a murine model of experimental asthma Translated title: Efecto del estrés prenatal en la regulación de la inflamación alérgica pulmonar en el modelo murino de asma experimental

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Devido ao seu rápido crescimento, o feto é particularmente vulnerável a insultos e modificações no millieu hormonal. Este fato sugere que situações adversas experimentadas pela mãe grávida podem alterar o desenvolvimento e a saúde da prole, explicado principalmente pela permeabilidade da barreira placentária a diversos hormônios e substâncias. O objetivo deste trabalho foi estudar o efeito do estresse pré-natal na regulação da inflamação alérgica pulmonar, empregando o modelo murino de asma experimental. Para este propósito foram utilizadas camundongas virgens da linhagem Swiss, com 50 dias de idade. Foi empregado o modelo de choque nas patas para promover o estresse pré-natal e o modelo do "metrô de Nova Efeito do estresse pré-natal na regulação da inflamação alérgica pulmonar no modelo murino de asma experimental 65 Iorque" para o estresse pós-natal. As fêmeas foram distribuídas em 4 grupos experimentais: CC: fêmeas não estressadas; CE: fêmeas estressadas pós-natalmente aos 60 dias de idade (PND60), EC: fêmeas nascidas de mães estressadas entre o dia 15 (GD15) e 18 de gestação (GD18); EE: fêmeas nascidas de mães estressadas entre o GD15 e GD18 e estressadas pós-natalmente aos PND60. A indução da inflamação alérgica pulmonar foi realizada através da sensibilização dos animais com solução de ovalbumina (OVA) 0,1 mg.Kg-1 sc para avaliação do leucograma, lavado broncoalveolar (BAL), celularidade hematopoiética medular e neuroquímica. Os experimentos foram realizados 24h após a última sessão de nebulização. O número de células do BAL foi significantemente maior nos animais do grupo EE, em relação àqueles dos grupos CC (P<0.01), CE (P<0.01) e EC (P<0.001). Na contagem diferencial do BAL os linfócitos e macrófagos do grupo EE foram significantemente maiores que em os outros grupos avaliados (P<0.05). Na contagem diferencial de células no sangue não foram observadas alterações (P>0.05) para os linfócitos, neutrófilos, eosinófilos e monócitos; porém, observou-se diferenças significativas (P<0.05) entre o número de bastonetes dos grupos, sendo maior nos animais do grupo CC em relação àqueles do grupo EC. O número de células hematopoiéticas da medula óssea foi significantemente (P<0.05) menor nos animais do grupo EE, em relação àqueles do grupo CC. No córtex pré-frontal, há diferenças significantes na relação Ácido Homovanílico/ Dopamina (HVA/DA) (P<0.05), sendo maior nos animais do grupo EC, em relação àqueles do grupo CE. Em conclusão, o estresse pré-natal levou a modulação de células do sistema imune (SI) dos neonatos, evidenciado após a exposição a estresse agudo pós-natal, amplificando a resposta alérgica pulmonar. Sugere-se que a maior susceptibilidade dos animais do grupo EE seja consequência de alterações induzidas pelo estresse pré-natal no eixo hipotálamo-pituitária-adrenal (HPA).

          Translated abstract

          Due to the rapid growth of the fetus it is particularly vulnerable to insults and changes in hormonal milieu. Therefore, is suggested that adverse situations experienced by the pregnant mother can alter the development and health of offspring, mainly due to the permeability of the placental barrier to various hormones and substances. The aim of the present investigation was to study the effects of prenatal stress in the regulation of pulmonary allergic inflammation, employing the murine model of experimental asthma. For this purpose, were used virgin female mice, Swiss lineage, of 50 days old. The models used were foot shock to induce prenatally stress, and "New York subway" stress to induce postnatally stress. Females were divided into 4 groups: CC group: not stressed females; CE group: postnatally stressed females (PND60); EC: females born from stressed mothers (GD15 to GD18); EE Group: females born from stressed mothers (GD15 to GD18) (footshock) and postnatally stressed (PND60). The induction of allergic pulmonary inflammation was done through sensitization of animals with 0,1 mg.Kg-1 sc of ovalbumin (OVA) solution, to further evaluate leukogram, bronchoalveolar lavage (BAL) hematopoietic marrow cellularity and neurochemistry. The experiments were performed 24 hours after the last session of nebulization. The number of BAL cells was significantly higher in EE group animals compared with the CC group (P<0.01), CE (P<0.01) and CE (P<0.001). In the differential count of the BAL, lymphocytes and macrophages of EE group were significantly higher than the other groups studied (P<0.05). In the blood differential cell count were not observed changes (P>0.05) for lymphocytes, neutrophils, eosinophils and monocytes; however, there were significant differences (P<0.05) observed in the number of rods cells between groups, being higher in animals the CC group compared to EC group. The number of hematopoietic cells of the bone marrow was significantly lower (P<0.05) in animals of Group EE, compared with CC group. In the prefrontal cortex, there were significant differences in homovanillic acid /dopamine (HVA/DA) (P<0.05) rate, being higher in the EC group, compared to EC group. In conclusion, prenatal stress modulated the immune system (SI) cells of neonates, evidenced after exposure to a post-natal acute stress by amplification of pulmonary allergic response. It is suggested that the increased susceptibility of animals EE group is a result of changes induced by prenatal stress on hypothalamus pituitary-adrenal (HPA) axis.

          Translated abstract

          Debido a su rápido crecimiento el feto es particularmente vulnerable a los cambios en el ambiente hormonal. Esto sugiere que situaciones adversas de la madre durante la gestación pueden alterar el desarrollo y la salud de la descendencia, principalmente debido a la permeabilidad de la barrera placentaria a diversas hormonas y sustancias. El objetivo del presente trabajo fue estudiar el efecto del estrés prenatal sobre la regulación de la inflamación alérgica pulmonar, empleando el modelo murino de asma experimental. Para este propósito fueron utilizadas ratonas vírgenes de linaje suizo de 50 d de edad. Fue empleado el modelo de descargas eléctricas en las patas (Footshock) para inducir el estrés prenatal y el modelo de estrés denominado "metro de Nueva York" para el estrés posnatal. Las hembras fueron divididas en 4 grupos experimentales: CC: hembras no estresadas; CE: hembras estresadas posnatalmente a los 60 d de edad (PND60); EC: hembras nacidas de madres estresadas entre el día 15 (GD15) y 18 de gestación (GD18); EE: hembras nacidas de madres estresadas entre el GD15 y GD18 y estresadas posnatalmente al PND60. La inducción de la inflamación alérgica pulmonar fue realizada a través de la sensibilización de los animales con solución de ovoalbúmina (OVA) 0,1 mg.Kg-1 sc. para posteriormente evaluar leucograma, lavado broncoalveolar (BAL), celularidad hematopoyética medular y neuroquímica. Los experimentos fueron realizados 24 horas después de la última sesión de nebulización. El número de células del BAL fue significativamente mayor en los animales del grupo EE, en comparación con los del grupo CC (P<0.01), CE (P<0.01) y CE (P<0.001). En el recuento diferencial del BAL, los linfocitos y macrófagos del grupo EE fueron significativamente más altos que los otros grupos estudiados (P<0.05). En el recuento diferencial de células en la sangre no fueron observadas alteraciones (P>0.05) para los linfocitos, neutrófilos, eosinófilos y monocitos; sin embargo, se observaron diferencias significativas (P<0.05) entre los grupos en el número de bastonetes, siendo mayor en los animales del grupo CC en relación al grupo EC. El número de células hematopoyéticas de la médula ósea fue significativamente menor (P<0.05) en los animales del Grupo EE, en comparación con los del grupo de CC. En la corteza prefrontal, hubo diferencias significativas en la relación Ácido Homovanílico/ Dopamina (HVA/DA) (P<0.05), siendo mayor en los animales del grupo EC, en comparación con los del grupo CE. En conclusión, el estrés prenatal produjo modulación de las células del sistema inmune (SI) de los neonatos, evidenciado después de la exposición a un estrés agudo posnatal, por la amplificación de la respuesta alérgica pulmonar. Se sugiere que la mayor susceptibilidad de los animales del grupo EE sea resultado de los cambios inducidos por el estrés prenatal en el eje hipotálamo-pituitaria-adrenal (HPA).

          Related collections

          Most cited references 53

          • Record: found
          • Abstract: found
          • Article: not found

          Acute stress enhances while chronic stress suppresses cell-mediated immunity in vivo: a potential role for leukocyte trafficking.

          Delayed type hypersensitivity (DTH) reactions are antigen-specific, cell-mediated immune responses which, depending on the antigen involved, mediate beneficial (resistance to viruses, bacteria, fungi, and certain tumors) or harmful (allergic dermatitis, autoimmunity) aspects of immune function. We have shown that acute stress administered immediately before antigenic challenge results in a significant enhancement of a skin DTH response in rats. A stress-induced trafficking or redeployment of leukocytes to the skin may be one of the factors mediating this immunoenhancement. Here we investigate the effects of varying the duration, intensity, and chronicity of stress on the DTH response and on changes in blood leukocyte distribution and glucocorticoid levels. Acute stress administered for 2 h prior to antigenic challenge, significantly enhanced the DTH response. Increasing the duration of stress from 2 h to 5 h produced the same magnitude enhancement in cutaneous DTH. Moreover, increasing the intensity of acute stress produced a significantly larger enhancement of the DTH response which was accompanied by increasing magnitudes of leukocyte redeployment. In contrast, chronic stress suppressed the DTH response when it was administered for 3 weeks before sensitization and either discontinued upon sensitization, or continued an additional week until challenge, or extended for one week after challenge. The stress-induced redeployment of peripheral blood lymphocytes was attenuated with increasing exposure to chronic stress and correlated with attenuated glucocorticoid responsivity. These results suggest that stress-induced alterations in lymphocyte redeployment may play an important role in mediating the bi-directional effects of acute versus chronic stress on cell-mediated immunity in vivo.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            The potential influence of maternal stress hormones on development and mental health of the offspring.

            Recent studies in humans suggest that alterations in the activity of the neuroendocrine system mediate the effects of psychosocial stress on fetal development and birth outcome. Chronic maternal distress compromises the normal regulation of hormonal activity during pregnancy and elevates free circulating corticotrophin-releasing hormone (CRH), probably of placental origin, before the normal increase occurs at term. Excess CRH, and other hormones like cortisol and met-enkephalin that pass through the placenta, could precipitate preterm labor, reduce birth weight and slow growth rate in prenatally stressed infants. CRH and/or cortisol have also been associated with impaired fetal habituation to stimuli and temperamental difficulties in infants. These changes may result from actions of the hormones on their receptors in the fetal limbic system. In the rat, gestational stress and excess maternal and fetal plasma corticosterone cause downregulation of fetal glucocorticoid (GR) and mineralocorticoid (MR) receptors and impair the feedback regulation of the hypothalamic-pituitary adrenal (HPA) axis in infancy and adulthood. The impairment in HPA axis activity can be prevented by maternal adrenalectomy and mimicked by administration of glucocorticoids. Gestational stress also increases CRH activity in the amygdala and the incidence of anxiogenic and depressive-like behavior in rats and non-human primates, which can be ameliorated by CRH antagonists. Excess amounts of CRH and cortisol reaching the human fetal brain during periods of chronic maternal stress could alter personality and predispose to attention deficits and depressive illness through changes in neurotransmitter activity.
              Bookmark
              • Record: found
              • Abstract: not found
              • Article: not found

              The role of adrenocorticoids as modulators of immune function in health and disease: neural, endocrine and immune interactions.

                Bookmark

                Author and article information

                Contributors
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Role: ND
                Journal
                rori
                ORINOQUIA
                Orinoquia
                Instituto de Investigaciones de la Orinoquia Colombiana (Meta, Villavicencio, Colombia )
                0121-3709
                December 2016
                : 20
                : 2
                : 64-77
                Affiliations
                São Paulo SP orgnameBioLab Brasil Brasil
                São Paulo SP orgnameUniversidade de São Paulo orgdiv1Instituto de Ciências Biomédicas orgdiv2Departamento de Anatomia Brasil
                São Paulo SP orgnameUniversidade Paulista orgdiv1Instituto de Ciências da Saúde Brasil vagnergjr@ 123456usp.br
                São Paulo SP orgnameUniversidade de São Paulo orgdiv1Faculdade de Medicina Veterinária e Zootecnia orgdiv2Departamento de Patologia Brasil
                São Paulo SP orgnameUniversidade Nove de Julho Brasil
                Villavicencio Meta orgnameUniversidad de los Llanos orgdiv1Facultad de Ciencias Agropecuarias y Recursos Naturales orgdiv2Instituto de Acuicultura Colombia
                Villavicencio Meta orgnameUniversidad de los Llanos orgdiv1Facultad de Ciencias Agropecuarias y Recursos Naturales orgdiv2Escuela de Ciencias Animales Colombia
                Article
                S0121-37092016000200009

                This work is licensed under a Creative Commons Attribution-NonCommercial 4.0 International License.

                Page count
                Figures: 0, Tables: 0, Equations: 0, References: 56, Pages: 14
                Product
                Product Information: website

                Comments

                Comment on this article