E. Gemmell et al., IMMUNOHISTOLOGICAL STUDY OF LESIONS INDUCED BY PORPHYROMONAS-GINGIVALIS IN A MURINE MODEL, Oral microbiology and immunology, 12(5), 1997, pp. 288-297
Citations number
45
Categorie Soggetti
Immunology,Microbiology,"Dentistry,Oral Surgery & Medicine
A previous study used a mouse model to demonstrate protection after ch
allenge with Porphyromonas gingivalis ATCC 33277. In the present study
, this same model was used to determine the phenotype of cells recruit
ed into the lesions during the course of the protective immune respons
e after immunization with this periodontal pathogen. BALB/c mice were
immunized with 100 mu g of P. gingivalis outer membrane antigens per m
ouse weekly for 3 weeks followed by challenge with live organisms 3 we
eks after the final immunization. Hematoxylin and eosin-stained sectio
ns showed inflammatory infiltrates in all lesions from control (immuni
zed with adjuvant only) and immunized mice. The lesions developed cent
ral necrotic cores surrounded by neutrophils, phagocytic macrophages a
nd lymphocytes. Neutrophils were the predominant cells in the lesions
1 day after challenge with significantly more in immunized than contro
l mice. Acid phosphatase and nonspecific esterase-positive macrophages
were detected at day 4 and became the predominant cells in the healin
g lesions. CD4- and CD8-positive T-cells were present from day 1, and
while numbers increased over time, there were no significant differenc
es in control or immunized mice. When mice were depleted of CD4 or CD8
cells prior to immunization with P. gingivalis, fewer neutrophils wer
e found in the lesions 1 day after challenge compared with undepleted
immunized mice. Acid phosphatase and nonspecific esterase-positive mac
rophages were not affected by T-cell depletion. The results suggest th
at the P. gingivalis-induced lesion in immunized BALB/c mice is consis
tent with a strong innate immune response involving the recruitment of
neutrophils in the first instance which may be under the control of T
cells. This is followed by the infiltration of phagocytic macrophages
which are involved in the healing process and do not appear to be reg
ulated by T cells.