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Immune response to cytolethal distending toxin of Aggregatibacter actinomycetemcomitans in periodontitis patients
Author(s) -
Ando E. S.,
DeGennaro L. A.,
Faveri M.,
Feres M.,
DiRienzo J. M.,
Mayer M. P. A.
Publication year - 2010
Publication title -
journal of periodontal research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.31
H-Index - 83
eISSN - 1600-0765
pISSN - 0022-3484
DOI - 10.1111/j.1600-0765.2009.01260.x
Subject(s) - aggregatibacter actinomycetemcomitans , cytolethal distending toxin , aggressive periodontitis , periodontitis , antibody , immune system , serotype , immunology , microbiology and biotechnology , medicine , biology , toxin , porphyromonas gingivalis , microbial toxins
Ando ES, De‐Gennaro LA, Faveri M, Feres M, DiRienzo JM, Mayer MPA. Immune response to cytolethal distending toxin of Aggregatibacter actinomycetemcomitans in periodontitis patients. J Periodont Res 2010; 45: 471–480. © 2010 John Wiley & Sons A/S Background and Objective: Cytolethal distending toxin (CDT) is a genotoxin produced by Aggregatibacter actinomycetemcomitans . In spite of its association with pathogenesis, little is known about the humoral immune response against the CDT. This study aimed to test whether subgingival colonization and humoral response to A. actinomycetemcomitans would lead to a response against CDT. Material and Methods: Sera from periodontally healthy, localized and generalized aggressive periodontitis and chronic periodontitis subjects ( n = 80) were assessed for immunoglobulin G titers to A. actinomycetemcomitans serotypes a/b/c and to each CDT subunit (CdtA, CdtB and CdtC) by ELISA. A. actinomycetemcomitans subgingival levels and neutralization of CDT activity were also analyzed. Results: Sera from 75.0% localized and 81.8% generalized aggressive periodontitis patients reacted to A. actinomycetemcomitans . A response to serotype b was detected in localized (66.7%) and generalized aggressive periodontitis (54.5%). Reactivity to A. actinomycetemcomitans correlated with subgingival colonization ( R = 0.75, p < 0.05). There was no correlation between A. actinomycetemcomitans colonization or response to serotypes and the immunoglobulin G response to CDT subunits. Titers of immunoglobulin G to CdtA and CdtB did not differ among groups; however, sera of all generalized aggressive periodontitis patients reacted to CdtC. Neutralization of CDT was not correlated with levels of antibodies to CDT subunits. Conclusion: Response to CdtA and CdtB did not correlate with the periodontal status of the subject in the context of an A. actinomycetemcomitans infection. However, a response to CdtC was found in sera of generalized but not of localized aggressive periodontitis subjects. Differences in response to CdtC between generalized and localized aggressive periodontitis subjects indicate that CDT could be expressed differently by the infecting strains. Alternatively, the antibody response to CdtC could require the colonization of multiple sites.