Artículos de revistas
Chlorella Vulgaris Treatment Ameliorates The Suppressive Effects Of Single And Repeated Stressors On Hematopoiesis
Registro en:
Brain, Behavior, And Immunity. , v. 29, n. , p. 39 - 50, 2013.
8891591
10.1016/j.bbi.2012.12.001
2-s2.0-84873459473
Autor
de Souza Queiroz J.
Barbosa C.M.V.
da Rocha M.C.
Bincoletto C.
Paredes-Gamero E.J.
de Souza Queiroz M.L.
Palermo Neto J.
Institución
Resumen
The reports regarding the mutual influence between the central nervous system and the immune system constitute a vast and somewhat controversial body of literature. Stress is known to disturb homeostasis, impairing immunological functions. In this study, we investigated the hematopoietic response of Chlorella vulgaris (CV)-treated mice exposed to single (SST) and repeated stress (RST). We observed a reduction in the numbers of hematopoietic progenitors (HP) in the bone marrow and long-term bone marrow cultures (LTBMC) using flow cytometry and a coinciding decrease in the number of granulocyte-macrophage colonies (CFU-GM) after treatment with both stressors, but SST caused a more profound suppression. We observed a proportional increase in the colony-stimulating activity (CSA) of the serum of animals subjected to SST or RST. In the bone marrow, SST and RST induced a decrease in both mature myeloid and lymphoid populations but did not affect pluripotent hematopoietic progenitors (Lin-Sca-1+c-kit+, LSK), and again, a more profound suppression was observed after SST. We further quantified the levels of interleukin-1α (IL-1α) and interleukin-6 (IL-6) and the number of myeloid cells in LTBMC. Both SST and RST reduced the levels of these cytokines to similar degrees. The myeloid population was also reduced in LTBMC, and SST induced a more intense suppression. Importantly, CV treatment prevented the changes produced by SST and RST in all of the parameters evaluated. Together, our results suggest that CV treatment is an effective tool for the prophylaxis of myelosuppression caused by single or repeated stressors. © 2012 Elsevier Inc. 29
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