Effect of Colchicine on Inducible Nitric Oxide Synthase Activity and Nitric Oxide Production of Mice Induced by <i>Aggregatibacter actinomycetemcomitans</i>

Abstract

Objective: Colchicine induced a non-protective Th 2-like immunity in Aggregatibacter actinomycetemcomitans-stimulated murine immune response. The aim of the present study was to determine whether colchicine affects inducible nitric oxide synthase (iNOS) activity and nitric oxide (NO) production in A. actinomycetemcomitans-immunized mice. Materials and Methods: BALB/c mice were sham-immunized (group I) or immunized with heat-killed A. actinomycetemcomitans (group II-VII). Colchicine was injected intraperitoneally before (group III), on the same day of (group IV), or after (group V) the primary immunization and on the same day of (group VI) or after (group VII) the secondary immunization. In vitro, spleen cells from either sham-or heat-killed A. actinomycetemcomitan-immunized animals were cultured and stimulated with heat-killed A. actinomycetemcomitans in the presence or absence of colchicine with or without addition of L-arginine, Db-cAMP, forskolin or interferon-γ (IFN-γ). The levels of splenic iNOS activity and both serum and culture supernatant NO levels were assessed. Results: The results showed that colchicine did inhibit both splenic iNOS activity and serum NO levels only when the drug was injected at the same time as the immunization (group IV and VI). Splenic iNOS activity and NO levels on antigen-stimulated spleen cell cultures were also suppressed by colchicine, even in the presence of L-arginine, Db-AMP or forskolin. IFN-γ only partially restored iNOS activity and NO levels in the antigen and colchicine-treated spleen cell cultures. Conclusion: This study suggests, therefore, that colchicine may suppress the iNOS activity and NO production in A. actinomycetemcomitans-immunized mice in vivo and in vitro.

The Carcinogenic Potential of Cadmium in Gingival Epithelium of Rats (Histological and Immunohistochemical Study)

“…Activation of iNOS leads to the production of large amounts of NO from inflammatory cells and also gingival cells for sustained periods of time (15) . As iNOS is expressed almost exclusively under inflammatory condition, this has led to the hypothesis that iNOS promotes the inflammatory response (12) . The aim of this research was to assess the carcinogenic effects of Cd, on the gingival tissue of albino rats, using histological and immunohistochemical examination.…”