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Humoral immune response to Aggregatibacter actinomycetemcomitans leukotoxin
Author(s) -
Brage M.,
Holmlund A.,
Johansson A.
Publication year - 2011
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.1600-0765.2010.01325.x
Subject(s) - aggregatibacter actinomycetemcomitans , antibody , immune system , periodontal pathogen , immunology , population , pathogen , medicine , aggressive periodontitis , western blot , microbiology and biotechnology , periodontitis , biology , porphyromonas gingivalis , biochemistry , environmental health , gene
Brage M, Holmlund A, Johansson A. Humoral immune response to Aggregatibacter actinomycetemcomitans leukotoxin. J Periodont Res 2011; 46: 170–175. © 2010 John Wiley & Sons A/S Background and Objective:  Periodontal disease is an inflammatory condition caused by bacterial infections that result in loss of the tooth supporting tissue. The periodontal pathogens produce virulence factors with capacity to affect the host immune response. Aggregatibacter actinomycetemcomitans is a periodontal pathogen that produces a leukotoxin that specifically affects human leukocytes. The aims of the present study were to examine the presence and function of systemic antibodies to the leukotoxin. Material and Methods:  One hundred and ninety‐seven middle‐aged (57 ± 5 years) Swedes with well‐documented periodontal status and medical factors related to cardiovascular diseases were studied. These data have been published previously. The serum samples were examined for the presence of leukotoxin antibodies by western blot and the capacity to neutralize leukotoxicity in an activity assay with leukotoxin and cultured leukemic cells. Results:  The results showed a high prevalence (57%) of antibodies against A. actinomycetemcomitans leukotoxin in the analyzed population. These antibodies were correlated with leukotoxin neutralizing capacity as well as with the ELISA titers of A. actinomycetemcomitans ‐specific IgA and IgG. In addition, high levels of leukotoxin antibodies were correlated with increasing age, but not with periodontal disease parameters or cardiovascular risk factors. Conclusion:  Systemic antibodies against A. actionmycetemcomitans leukotoxin were common in this adult Swedish population. These antibodies might contribute to limit the systemic effects of the infection.

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