Galectin-1 localizing in gingival tissues regulates macrophage cytokine mRNA expression

Objectives: Galectin-1, a beta galactoside binding protein, has been proved to improve injured peripheral nerve tissues by stimulating macrophages. In this paper we demonstrated localization and a role of galectin-1 in gingival tissues using a stress model rat, P. gingivalis and cultured macrophages.

Methods: We used restraint stress rats created by enclosing them in a flexible wire mesh bend to fit its body. P. gingivalis ATCC 33277 (P.g) was used for infection. Localization of galectin-1 in rat gingival tissues was identified by an immunohistochemical method with anti-galectin-1 antibody. mRNA expressions of galectin-1 in examined rat gingival tissues were analyzed by RT-PCR. Effects of conditioned media from cultured P.g and oxidized galectin-1 on mRNA expressions of cytokines (IL-1â, IL-6, LIF, iNOS) in cultured peritoneal macrophages were examined for three different incubation times, 2, 4, and 6 hours and analyzed by RT-PCR.

Result: The immunohistochemical analysis revealed that galectin-1 localized in gingival tissues. Although alveolar bone loss was scarcely seen in the stress rat, P.g infected rats clearly showed alveolar bone loss. Furthermore, the addition of the stress to P.g infected rats advanced the bone loss. This change of bone loss severity was closely related to the increase of the galectin-1 expression. A P.g conditioned medium promoted mRNA expressions of IL-1â, LIF, and iNOS. An addition of oxidized galectin-1 enhanced mRNA expressions of IL-1â, IL-6, LIF and iNOS only at 4 hours incubation.

Conclusion: Galectin-1 localized in gingival tissues and its mRNA expression was closely related to the severity of alveolar bone loss caused by the restraint stress and P.g infection. This factor also regulated cytokine expressions in the presence of P.g conditioned medium. These results indicate that galectin-1 may be one of the regulatory factors in periodontal diseases.

MEXT provided an Open Research Center subsidy to support this work.