Antibody responses to Porphyromonas gingivalis infection in a murine abscess model--involvement of gingipains and responses to re-infection.
BACKGROUND
Porphyromonas gingivalis is one of the most important periodontopathogens. It produces cysteine proteinases named gingipains. We previously examined the effect of gingipains on abscess formation in a murine model. The rgpA rgpB double and kgp mutants induced smaller abscesses than the wild type. Moreover, the rgpA rgpB kgp triple (gingipain-null) mutant hardly showed lesion formation at all under the experimental conditions used, indicating that genes encoding gingipains are important for P. gingivalis virulence.


OBJECTIVE
Here, we further report the humoral immune responses induced by P. gingivalis strains.


METHODS
After the lesions were apparently cured, sera were collected from the mice and immunoglobulin G (IgG) responses against the whole cell antigens of wild-type P. gingivalis were measured.


RESULTS
Wild-type strain was found to induce a strong antibody reaction. On the other hand, the rgpA rgpB kgp triple and kgp mutants induced significantly lower antibody responses compared to the wild type. Western blotting analysis confirmed the differences in antibody production. Next, these mice were re-infected with wild-type strain. Mice that were first infected with wild-type strain showed significantly smaller lesion formation than control mice that were first infected with medium only. On the other hand, mice that were first infected with mutant strains devoid of gingipain activities did not show resistance to re-infection and immunoglobulins directed against gingipains may be protective.


CONCLUSIONS
These results suggest that gingipains play an important role in abscess formation in mice, and humoral immune responses seem to be partly responsible for the resistance to re-infection by P. gingivalis.
Yoneda
Masahiro
M
Section of Periodontology, Department of Oral Rehabilitation, Faculty of Dental Science, Graduate School of Kyushu University, Japan. yoneda@dent.kyushu-u.ac.jp
Hirofuji
Takao
T
Motooka
Noriko
N
Anan
Hisashi
H
Hamachi
Takafumi
T
Miura
Mayumi
M
Ishihara
Yoshihisa
Y
Maeda
Katsumasa
K
D000038:Abscess / Q000276:immunology*; D018829:Adhesins, Bacterial / Q000235:genetics / Q000276:immunology*; D000818:Animals; D000907:Antibodies, Bacterial / Q000097:blood / Q000276:immunology*; D000942:Antigens, Bacterial / Q000276:immunology; D016866:Bacteroidaceae Infections / Q000276:immunology*; D003546:Cysteine Endopeptidases / Q000235:genetics / Q000276:immunology*; D004195:Disease Models, Animal; D004198:Disease Susceptibility / Q000276:immunology; D005260:Female; D000080867:Gingipain Cysteine Endopeptidases; D006388:Hemagglutinins / Q000235:genetics / Q000276:immunology*; D007074:Immunoglobulin G / Q000097:blood / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D008815:Mice, Inbred Strains; D009154:Mutation / Q000235:genetics; D016966:Porphyromonas gingivalis / Q000201:enzymology / Q000276:immunology*; D014774:Virulence / Q000235:genetics
D018829:Adhesins, Bacterial; D000907:Antibodies, Bacterial; D000942:Antigens, Bacterial; D000080867:Gingipain Cysteine Endopeptidases; D006388:Hemagglutinins; D007074:Immunoglobulin G; D003546:Cysteine Endopeptidases