Inhibitory effect of galectin‐3 on the cytokine‐inducing activity of periodontopathic Aggregatibacter actinomycetemcomitans endotoxin in splenocytes derived from mice

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.