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Keywords:

  • galectin-3;
  • cytokines;
  • periodontopathic bacteria;
  • endotoxin

Abstract

Galectins, a family of animal lectins, are involved not only in development and differentiation but also in immunoregulation and host–pathogen interactions. Galectin-3 interacts with lipopolysaccharides in gram-negative bacteria such as Escherichia coli, Salmonella minnesota and Pseudomonas aeruginosa. The present study investigated whether galectin-3 inhibited the cytokine-inducing activity of periodontopathic bacterial lipopolysaccharides using splenocytes derived from mice of different ages. Lipopolysaccharides were extracted from Aggregatibacter actinomycetemcomitans Y4 and Porphyromonas gingivalis ATCC 33277, and then purified. Enzyme-linked immunosorbent assay (ELISA) analysis revealed that galectin-3 adhered to A. actinomycetemcomitans lipopolysaccharides, but not to the lipopolysaccharides of P. gingivalis. Splenocytes were prepared from 1- or 7-month-old C57BL/6 mice. Either A. actinomycetemcomitans lipopolysaccharides (200 ng mL−1) alone or lipopolysaccharides and murine galectin-3 (10 μg mL−1) were added to culture solutions, and the release of interleukin-6 (IL-6) and interferon-γ (IFNγ) from splenocytes was measured by ELISA after a 17-h incubation. In all mice tested, A. actinomycetemcomitans lipopolysaccharide stimulation significantly increased the production of IL-6 and IFNγ (P<0.01). Murine galectin-3 suppressed lipopolysaccharide-induced cytokine production in the splenocytes of the 1-month-old mice (P<0.02 for IL-6; P<0.05 for IFNγ), but not in the splenocytes of the 7-month-old mice. This suggests that responses change with age.