In vivo dehydroepiandrosterone restores age-associated defects in the protein kinase C signal transduction pathway and related functional responses.

作者: Emanuela Corsini , Laura Lucchi , Massimo Meroni , Marco Racchi , Bruno Solerte

DOI: 10.4049/JIMMUNOL.168.4.1753

关键词: HormoneIn vivoDehydroepiandrosteroneInternal medicineProtein kinase ASignal transductionReceptorBiologyEndocrinologyAlveolar macrophageKinase

摘要: Elderly subjects are at increased risk of pneumonia, influenza, and tuberculosis. Besides the known age-related decrease in mechanisms for mechanical clearance lungs, impaired alveolar macrophage function contributes to illness elderly. We have previously shown that age-induced immunodeficiencies associated with a defective system anchoring protein kinase C. Castration young male rats produces effects on macrophages similar those aging, suggesting relationship between circulating sex hormones, particularly androgens, decreases receptor activated C (RACK-1) observed. The aging process humans is decline plasma concentrations dehydroepiandrosterone (DHEA) its sulfate, among other steroid hormones. report here vitro vivo administration DHEA restores age-decreased level RACK-1 LPS-stimulated production TNF-α macrophages. also spleen mitogenic responses expression. These findings suggest loss immunological responses, linked pathways signal transduction, partially under hormonal control can be restored by appropriate replacement therapy.

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