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  • Open Access

Modulation of spontaneous proliferation of T-lymphocytes from HTLV-1- infected individuals by quinoline compounds

  • 1,
  • 1,
  • 2,
  • 1, 3 and
  • 1Email author
Retrovirology201411 (Suppl 1) :P121

https://doi.org/10.1186/1742-4690-11-S1-P121

  • Published:

Keywords

  • Cell Proliferation
  • Transmission Electron Microscope
  • Serial Concentration
  • Mononuclear Cell
  • Peripheral Blood Mononuclear Cell

Spontaneous proliferation, a hallmark of Human-T Lymphocyte Virus Type 1 (HTLV-1) infection, is particularly higher in HAM/TSP patients compared to asymptomatic carriers. However the role of the proliferation in the pathogenesis of HAM/TSP is still unknown. The identification of drugs that modulate the spontaneous proliferation may be important for the treatment of HAM/TSP disease. We have evaluated the effect of three different quinoline compounds (A, B and C) on the modulation of spontaneous proliferation of peripheral blood mononuclear cells from HTLV-1 patients with HAM/TSP. The cells from 8 HAM/TSP patients were cultivated in the presence of serial concentrations of quinolone compounds. Cell proliferation was assessed by 3[H]thymidine incorporation. Cell viability was measured by optical density in the presence of MTT. The ultrastructure analysis was done using a transmission electron microscope. Quinoline compounds were not toxic at the concentrations evaluated. The IC50 was 18.5 µM for compound A, 30.5 µM for compound B and 3.4 µM for compound C. The three compounds inhibited more than 90% of spontaneous proliferation. Cultured cells in the presence of quinolone compounds showed vacuoles presented with myelin-like membranes, probably autophagic vacuole-like compartments, observed by electronic microscopy. In conclusion, the quinoline compounds showed no toxicity and were able to inhibit the spontaneous proliferation of T cells from HTLV-1-infected individuals. New assessments are being applied to understand how the quinoline compounds act on cells by decreasing cell proliferation.

Authors’ Affiliations

(1)
Gonçalo Moniz Research Center - CPqGM/FIOCRUZ, Salvador, Ba, Brazil
(2)
Faculté de Pharmacie, rue J. B. Clément, Châtenay-Malabry Cedex, France
(3)
Bahiana School of Medicine and Public Health, Brazil

Copyright

© Pinto et al; licensee BioMed Central Ltd. 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.

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