Protective immunity to Porphyromonas gingivalis infection in a murine model.
The mouse abscess model has been used extensively to demonstrate protection after challenge with periodontopathic organisms. In the present study, an outer membrane (OM) preparation of P. gingivalis ATCC 33277 was used to immunize BALB/c mice prior to challenge with live P. gingivalis organisms. This OM preparation, particularly at the highest dose level of 100 micrograms/immunization, was able to induce high levels of specific antibody and subsequent protective immunity. Protection in all immunized mice was noted by the rapid healing of the primary lesions, a low incidence of secondary lesions, and, in the highest dose group, an absence of septicemia. Non-immunized animals demonstrated a slower development as well as healing of primary lesions, with higher numbers and larger sizes of secondary lesions. Weight loss and behavior patterns such as hunched bodies, ruffled hair, and stiffness of the hind legs were particularly noted in this group. Depletion of CD4 T cells in mice prior to immunization with 100 micrograms P. gingivalis OM resulted in significantly depressed serum levels of anti-P. gingivalis antibody and an increase in the physical signs of disease compared with both the immunized and control groups. Western blot analysis demonstrated three antigen bands (63.3, 50.1, and 45.1) recognized by all immunized groups and also the control non-immunized group, although the latter recognition occurred only after challenge. A further antigen band of 36.1 kDa was recognized by sera from the highest dose group only. This study has demonstrated the ability of P. gingivalis OM to provide protection against challenge with live P. gingivalis organisms. The increased physical signs of disease seen in the CD4 depleted animals compared with the control group not only illustrate the protective role of serum antibody, but also suggest a possible role for T cell mechanisms in control of the lesion locally. The ability of specific OM antigens to provide similar protective immunity remains to be ascertained.
Bird
P S
PS
Department of Dentistry, University of Queensland, Australia.
Gemmell
E
E
Polak
B
B
Paton
R G
RG
Sosroseno
W
W
Seymour
G J
GJ
D000704:Analysis of Variance; D000818:Animals; D000907:Antibodies, Bacterial / Q000096:biosynthesis / Q000097:blood; D000942:Antigens, Bacterial / Q000302:isolation & purification; D001425:Bacterial Outer Membrane Proteins / Q000276:immunology; D001428:Bacterial Vaccines; D016866:Bacteroidaceae Infections / Q000276:immunology / Q000517:prevention & control*; D015153:Blotting, Western; D018791:CD4 Lymphocyte Count; D004591:Electrophoresis, Polyacrylamide Gel; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D010508:Periodontal Abscess / Q000276:immunology / Q000382:microbiology / Q000517:prevention & control*; D016966:Porphyromonas gingivalis / Q000276:immunology*; D014611:Vaccination
D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D001425:Bacterial Outer Membrane Proteins; D001428:Bacterial Vaccines