Functional properties of nonhuman primate antibody to Porphyromonas gingivalis.
The nonhuman primate (NHP) serves as a useful model for examining the host-parasite interactions in Porphyromonas gingivalis-associated periodontal disease. This study determined the influence of NHP sera on (i) the direct killing of P. gingivalis, (ii) P. gingivalis-induced superoxide anion (O2-) release from human polymorphonuclear leukocytes (PMNs), and (iii) the ability of PMNs to bind and phagocytize P. gingivalis. Three types of NHP sera were utilized: (i) normal or baseline sera; (ii) sera obtained after ligature-induced periodontitis; and (iii) sera obtained following active immunization with formalinized P. gingivalis. All assays were performed with or without the addition of human complement. Significantly more (P < 0.01) direct killing of P. gingivalis occurred with immunized sera and complement than with any of the other treatments. The sera from ligature-induced periodontitis NHPs had significantly less (P < 0.03) killing capacity than the baseline sera, which contained natural antibody produced to P. gingivalis colonization. Sera from immunized NHPs were used to opsonize P. gingivalis and caused significantly greater (P < 0.01) levels of O2- release from PMNs. Finally, the sera from immunized NHPs significantly enhanced (P < 0.009) the uptake of P. gingivalis by PMNs, although binding of the bacteria to PMNs was similar among all three serum types. Active immunization of NHPs with P. gingivalis elicited a functional antibody that enhanced direct killing, positively influenced the activation of PMNs, and enhanced the ability of PMNs to phagocytize P. gingivalis. Moreover, antibody produced as a sequela of progressing periodontitis appeared to lack these functions. A wide variability in functional capacity of the sera from individual NHPs, which may contribute to an individual's susceptibility to P. gingivalis-induced disease, was noted. This variability suggested that results from functional tests of serum antibody may aid in predicting host susceptibility to disease and response to therapy.
Anderson
D M
DM
Department of Periodontics, University of Texas Health Science Center at San Antonio 78284, USA.
Ebersole
J L
JL
Novak
M J
MJ
D000328:Adult; D000818:Animals; D000907:Antibodies, Bacterial / Q000096:biosynthesis / Q000276:immunology*; D003165:Complement System Proteins / Q000276:immunology; D005260:Female; D006801:Humans; D008252:Macaca fascicularis; D009504:Neutrophils / Q000378:metabolism; D016966:Porphyromonas gingivalis / Q000276:immunology*; D013481:Superoxides / Q000378:metabolism
D000907:Antibodies, Bacterial; D013481:Superoxides; D003165:Complement System Proteins