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dc.creatorHernández-Pando, R.
dc.creatorDe la Luz Streber, M.
dc.creatorOrozco, H.
dc.creatorArriaga, K.
dc.creatorPavón, L.
dc.creatorAl-Nakhli, S.A.
dc.creatorRook, G.A.W.
dc.date.accessioned2017-06-29T04:21:16Z
dc.date.available2017-06-29T04:21:16Z
dc.date.issued1998es_ES
dc.identifier260es_ES
dc.identifier.issn0019-2805es_ES
dc.identifier.urihttp://repositorio.inprf.gob.mx/handle/123456789/4954
dc.identifier.urihttps://doi.org/10.1046/j.1365-2567.1998.00601.xes_ES
dc.language.isoenges_ES
dc.relation95 (2) 234-241 p.es_ES
dc.relationversión del editores_ES
dc.rightsacceso cerradoes_ES
dc.titleThe effects of androstenediol and dehydroepiandrosterone on the course and cytokine profile of tuberculosis in BALB/c micees_ES
dc.typearticlees_ES
dc.contributor.affiliationExperimental Pathology Laboratory, Department of Pathology, Instituto Nacional de la Nutricion 'Salvador Zubiran', Mexico City, Mexico.es_ES
dc.relation.jnabreviadoIMMUNOLOGYes_ES
dc.relation.journalImmunologyes_ES
dc.identifier.placeInglaterraes_ES
dc.date.published1998es_ES
dc.identifier.organizacionInstituto Mexicano de Psiquiatríaes_ES
dc.identifier.eissn1365-2567es_ES
dc.identifier.doi10.1046/j.1365-2567.1998.00601.xes_ES
dc.description.monthOctes_ES
dc.description.abstractotrodiomaImmunity to Mycobacterium tuberculosis requires a T helper 1 (Th1) cytokine balance accompanied by tumour necrosis factor-_ (TNF-_), and activated macrophages. These facets of the immune response are sensitive to suppression by glucocorticoids (GC), which can reactivate and exacerbate tuberculosis in man and animals. Dehydroepiandrosterone (DHEA) and its derivative, 3_,17_ androstenediol (AED), are reported to have antiglucocorticoid properties in vivo. We therefore investigated the effects of predetermined optimal doses of these compounds, on the course of pulmonary tuberculosis in an established model in BALB-c mice in which an early phase of Th1-mediated response accompanied by adrenal hyperplasia, is followed by a switch to Th2, progressive loss of TNF-_ expression and disease progression. Both compounds were protective, particularly AED which caused a fall in bacterial counts and prolonged survival. These effects correlated with the appearance within 3 days of cellular infiltrates rich in cells expressing interleukin-2 (IL-2), IL-1_ and TNF-_, and with partial suppression of the switch to IL-4 producing cells that occurred in controls. AED also caused enhanced development of granulomas at 14 days, and persistence of granuloma formation to 120 days, with a corresponding suppression of areas affected by pneumonia. Much of the therapeutic effect of AED and DHEA was obtained by treating for only the first 3 weeks, which is the phase of adrenal hyperplasia. These results suggest that the ratio of GC to anti-GC steroids may play a role in the pathogenesis of tuberculosis, and further investigation could lead to novel treatment strategies.es_ES
dc.subject.koAndrostenediol-Therapeutic usees_ES
dc.subject.koAnimalses_ES
dc.subject.koColony Count, Microbiales_ES
dc.subject.koCytokines-Analysises_ES
dc.subject.koCytokines-Metabolismes_ES
dc.subject.koDehydroepiandrosteronees_ES
dc.subject.koImmunohistochemistryes_ES
dc.subject.koInterleukin-1es_ES
dc.subject.koInterleukin-2es_ES
dc.subject.koLung-Pathologyes_ES
dc.subject.koMalees_ES
dc.subject.koMicees_ES
dc.subject.koTime Factorses_ES
dc.subject.koTuberculosis, Pulmonary-Drug therapyes_ES
dc.subject.koimmunology-Microbiologyes_ES
dc.subject.koTumor Necrosis Factor-alphaes_ES
dc.subject.koDehydroepiandrosteronees_ES


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