Effect of immunization on experimental Bacteroides gingivalis infection in a murine model

Abstract

BALB/c mice were immunized with an invasive (A7A1-28) or noninvasive (381) Bacteroides gingivalis strain, Bacteroides intermedius, or Ringer solution. All immunized mice were subsequently challenged with the invasive B. gingivalis strain and examined for septicemia or secondary spread of the infection or both. Mice immunized with the invasive B. gingivalis strain localized the infection to the challenge site. Mice immunized with the noninvasive B. gingivalis strain, B. intermedius, or Ringer solution developed spreading infections. These data suggest that immunization with an invasive B. gingivalis strain can alter the course of subsequent infections. Anaerobic bacteria such as Bacteroides species are prevalent in infections characterized by suppuration and abscess formation (1). Bacteroides gingivalis is a gram-negative oral bacterium that has been associated with adult periodontal disease (14-17, 19, 22, 24) and abscesses of oral origin (2, 8, 20). Previous studies have demonstrated heterogeneity of virulence among different B. gingivalis isolates in mice (6, 10, 18), and guinea pigs (5, 6). Some strains produce a localized abscess at the injection site, while others spread to distant sites and may produce septicemia and death. Therefore, based on its pathogenesis in animal models, B. gingivalis can be classified as invasive or noninvasive. The role of prior immunization in modifying the response to experimental infection has been examined by using the murine model. For example, mice infected with Bacteroides fragilis can be protected from disease by immunization (11-13, 23). The present study was performed to determine whether immunization with B. gingivalis could protect mice from abscess formation or secondary spread of the infection or both after challenge with an invasive B. gingivalis isolate. An invasive and a noninvasive B. gingivalis strain were used in this study. B. gingivalis 381 (courtesy of S. S. Socransky, Forsyth Dental Center) was isolated from an adult with periodontitis. Previous studies in our laboratory have shown that this strain induces localized abscesses in mice and does not produce a secondary lesion (10). It is categorized as noninvasive. B. gingivalis A7A1-28, an invasive strain, was isolated in 1985 at the State University of New York at Buffalo from a 9-mm pocket in a 37-year-old male periodontitis patient with non-insulin-dependent diabetes mellitus. In mice, this B. gingivalis isolate produces ulcerated lesions distant from the injection site, septicemia, and often death (10). The pathogenic potential of this strain is similar to that described for strains W50 and W83 by Van Steenbergen et al. (18). Bacteroides intermedius ATCC 25261, obtained from the American Type Culture Collection, Rockville, Md., was used as a control. All bacteria were cultured on tryptic soy agar (Difco Laboratories, Detroit, Mich.) supplemented with 5% sheep blood (Crane Laboratories, Inc., Syracuse, N.Y.), 5 ,ug of hemin (Sigma Chemical Co., St. Louis, Mo.) per ml, 0.5 ,ug of menadione * Corresponding au...

Strain‐dependent activation of the mouse immune response is correlated with Porphyromonas gingivalis‐induced experimental periodontitis

“…The specific P. gingivalis strains were chosen due to their heterogenic virulence properties. For example, P. gingivalis 381 has only a moderate proteolytic activity (Birkedal-Hansen et al 1988, Neiders et al 1989) and does not produce disseminated disease when injected subcutaneously into mice (Van Steenbergen et al 1982, Chen et al 1987), while P. gingivalis 53977 is more proteolytic (Birkedal-Hansen et al 1988, Neiders et al 1989) and may produce widespread infection, cachexia and death (Chen et al 1987, Neiders et al 1989. Two of these strains also show different patterns with respect to the induction of gingival collagenase and gellatinase activity; P. gingivalis 53977 induced high hostcollagenase and gellatinase activity 42 days after infection, while only moderate activity was induced by P. gingivalis 381 (Evans et al 1992).…”

Synergistic biofilm formation byTreponema denticolaandPorphyromonas gingivalis

“…4). Quantification of synergistic biofilm formation by P. gingivalis 381 mutants G102 (rgpB), G102W (rgpB, kgp), JH007 (fimA) and the abscess forming strains 53977 and W50 [17,18] revealed significant attenuation compared with P. gingivalis 381. However, the percent coaggregation of strains G102, G102W, and JH007 did not parallel the results of biofilm formation as their coaggregation rates were quite similar to that exhibited by P. gingivalis 381.…”

The Effects of Interleukin‐10 Depletion In Vivo on the Immune Response to Porphyromonas gingivalis in a Murine Model

“…A murine abscess model induced by P. gingivalis to delineate the immune response to this periodontopathogen has been well established. [18][19][20][21] Our previous studies have shown that the P. gingivalis-induced murine immune response is dependent upon CD4 cells, since in vivo depletion of this T cell subset prior to immunization suppressed both antigen-specific cellular and humoral immune responses. 20,21 The infiltrating cells in the P. gingivalis-induced lesions in this murine model had the same phenotypes as those of the inflamed gingiva of periodontally diseased patients, 21 which demonstrated the usefulness of this animal model.…”