Premium
Antibody Responses to Porphyromonas gingivalis Hemagglutinin A and Outer Membrane Protein in Chronic Periodontitis
Author(s) -
Kobayashi Tetsuo,
Kaneko Susumu,
Tahara Tomoyuki,
Hayakawa Mitsuo,
Abiko Yoshimitsu,
Yoshie Hiromasa
Publication year - 2006
Publication title -
journal of periodontology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.036
H-Index - 156
eISSN - 1943-3670
pISSN - 0022-3492
DOI - 10.1902/jop.2006.050138
Subject(s) - porphyromonas gingivalis , hemagglutinin (influenza) , chronic periodontitis , periodontitis , microbiology and biotechnology , bacterial outer membrane , bacteroidaceae , antibody , chemistry , medicine , biology , immunology , dentistry , bacteria , biochemistry , gene , escherichia coli , genetics
Background: Hemagglutinin and outer membrane protein (OMP) are major virulence factors associated with colonization of Porphyromonas gingivalis in the gingival crevice. The genes for the 200‐kDa antigenic protein (200‐kDa AP) and 40‐kDa OMP of P. gingivalis have been successfully cloned. Additionally, the 200‐kDa AP gene has been shown to constitute the hemagglutinin A (hagA) gene of P. gingivalis . Therefore, this study was constructed to evaluate the distributions and serum levels of immnoglobulin G (IgG) antibodies specific for 200‐kDa AP and 40‐kDa OMP in periodontitis patients. Methods: Fifty patients with chronic periodontitis and 59 controls without periodontal destruction were enrolled in this study. We cloned the genes for 200‐kDa AP and 40‐kDa OMP from P. gingivalis and constructed the purified recombinant proteins. Serum levels of IgG subclass antibodies specific for both recombinant 200‐kDa and 40‐kDa OMP were determined in patients and controls by an enzyme‐linked immunosorbent assay (ELISA). Results: The serum IgG subclass distribution for patients and controls was IgG1 > IgG4 > IgG2 > IgG3 in the anti‐200‐kDa AP response, which was almost identical to that in the anti‐40‐kDa OMP response. The patient group showed significantly higher serum IgG responses to the 40‐kDa OMP than the control group ( P <0.01). In contrast, IgG subclass responses to the 200‐kDa AP were not different between the patients and controls. Serum levels of antibodies reactive with both 200‐kDa and 40‐kDa proteins did not have a significant association with mean probing depth. Conclusion: These results suggested that serum IgG responses against P. gingivalis OMP rather than the hagA may be more active in chronic periodontitis.