Kojic acid, a secondary metabolite from Aspergillus sp., acts as an inducer of macrophage activation

Authors

  • Ana Paula D. Rodrigues,

    1. Universidade Federal do Par, Instituto de Cincias Biolgicas, Laboratrio de Biologia Estrutural, Belm, Par, Brazil
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  • Antônio Sergio C. Carvalho,

    1. Universidade Federal do Par, Instituto de Cincias Exatas e Naturais, Laboratrio Desenvolvimento e Planejamento de Frmacos, Belm, Par, Brazil
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  • Alberdan S. Santos,

    1. Universidade Federal do Par, Instituto de Cincias Exatas e Naturais, Laboratrio Desenvolvimento e Planejamento de Frmacos, Belm, Par, Brazil
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  • Claudio N. Alves,

    1. Universidade Federal do Par, Instituto de Cincias Exatas e Naturais, Laboratrio Desenvolvimento e Planejamento de Frmacos, Belm, Par, Brazil
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  • José Luiz M. do Nascimento,

    1. Universidade Federal do Par, Instituto de Cincias Biolgicas, Laboratrio de Neuroqumica Molecular e Celular, Belm, Par, Brazil
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  • Edilene O. Silva

    Corresponding author
    1. Universidade Federal do Par, Instituto de Cincias Biolgicas, Laboratrio de Biologia Estrutural, Belm, Par, Brazil
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To whom correspondence should be addressed (email edilene@ufpa.br).

Abstract

KA (kojic acid) is a secondary metabolite isolated from Aspergillus fungi that has demonstrated skin whitening, antioxidant and antitumour properties among others. However, limited information is available regarding its effects on macrophages, the major cell involved in cell defence. The aim of the present study was to analyse whether KA affects functional properties related to macrophage activation, such as phagocytosis and spreading ability over a substrate. Treatment of resident macrophages with 50 μg/ml KA for 1 h induced both morphological and physiological alterations in cells. Immunofluorescence microscopy revealed enhanced cell spreading and an increase in cell surface exposure, associated with a rearrangement of microtubules, actin filaments and intermediate filaments. KA also potentiated phagocytosis by macrophages, as demonstrated by the increase in phagocytic activity towards yeast, when compared to untreated cells. KA increased the production of ROS (reactive oxygen species), but not NO (nitric oxide) production. Three tests were used to assess cell viability; MTT [3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide], NR (neutral red) uptake and PI (propidium iodide) exclusion test, which showed that macrophages maintain their viability following KA treatment. Results indicate that KA can modulate macrophage activation through cytoskeleton rearrangement, increase cell surface exposure, enhance the phagocytic process and ROS production. The study demonstrates a new role for KA as a macrophage activator.

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