Abstract
Anti-P. gingivalis immune sera were obtained from mice immunized with either P. gingivalis alone, or F. nucleaturm followed by P. gingivalis. Two groups of immune sera were examined for binding capacity to P. gingivalis biofilm by confocal laser scanning microscope, Antibody avidity index was also determined for each immune sera. The results indicated that prior immunization of mice with F. nucleaturm impaired P. gingivalis-specific immune sera in binding capacity to biofilm and antibody avidity to P. gingivalis. Elevated antibody responses in patients with destructive periodontal disease has often been related to suboptimal level of protective antibody $(opsonophagocytosis)^{1-3)}$ while post-immune sera obtained with experimental animals using a single periodontal pathogen demonstrated satisfactory levels of protective function against the homologous bacterial $challenge^{4,5)}$.The reason is unclear why elevated IgG responses in periodontal patients to periodontal pathogens do not necessarily reflect their protective function. Such an immune deviation might be derived from the fact that destructive periodontal disease is cumulative result of immunopathologic processes responding to an array of different colonizing microorganisms sequentially infecting in the subgingival environmental niche. Fusobacterium nucleaturm is one of the key pathogens in gingivitis, in the transitional phase of conversion of gingivitis into destructive periodontitk, and in adult $periodontitis^{6-8)}$. It also plays a central role in coaggregation with other important microbial species in subgingival $area^{6,9,10)}$ as well as in $biofilm^{11)}$, especially with Porphyromonas gingjvalis in synergism of virulence in human periodontal disease or in animal $models^{12-14)}$. This organism has also been reported to have immune modulating activity for secondary immune response to Actinobacillus $actinomycetemcomitans^{15)}$. It is presumed that sequential colonization and intermicrobial coaggregation between intermediate and late colonizers could potentially modulate the immune responses and development of specific T cell phenotypes in periodontal lesions. We have recently demonstrated the skewed polarization of P. gingivalis-specific helper T cell clones in mice immunized with F. nucleaturm followed by P. $gingivalis.^{16)}$. Consequently F. nucleaturm may initially prime the immune cells and modify their responses to the successive organism, P. gingivalis. This could explain why one frequently observes non-protective serum antibodies to P. gingivalis in periodontal patients in contrast with those obtained from animals that were immunized with $P.gingivalis\;alone^{17)}$. The present study was performed to investigate the immune modulating effect of F. nucleatum on serum binding to experimental biofilms and the avidity of anti-P. gingivalis antibody.
P. gingivalis를 단독면역하거나 또는 Fusobacterium nucleatum 선면역 후 P. gingivalis 항혈청을 각각 얻어냈다. 두 종류의 항혈청이 P. gingivalis biofilm을 침투해 들어가는 능력을 confocal laser scanning microscope를 이용하여 비교 감증하였다. 항혈청의 P. gingivalis에 대한 avidity index도 측정하였다. 결과적으로 F. nucleatum의 선면역은 P. gingivalis 특이 항혈청에 대해 세균성 biofilm의 침투능력을 저하시키고, 동일한 세균에 대한 avidity도 감소시켰다.