Longitudinal human serum antibody responses to outer membrane antigens of Actinobacillus actinomycetemcomitans

Jeffrey L. Ebersole, Michelle J. Steffen, David Cappelli

Research output: Contribution to journalArticle

10 Citations (Scopus)

Abstract

We hypothesize that serum antibody responses to antigens of a periodontopathogen would vary temporally and that the specificity of these host antibodies would relate to infection and disease activity. To test the hypothesis, we obtained between 6 and 13 serum samples from Actinobacillus actinomycetemcomitans (Aa)-positive (serological and microbiological) periodontitis patients at time points between 18 and 42 months into the study, and evaluated specific antibody responses to outer membrane antigens (OMA) of Aa strain Y4. Sera from these patients detected 22 different OMA. Early-onset (EOP; n=7) and adult (AP; n=11) periodontitis patients responded to 35% and 41% of the OMA, respectively. 2 of 9 sera from healthy subjects detected no antigens and 7/9 sera detected 7% of the OMA (p<0.0001 versus EOP and AP). The frequency of antibody responses to the 17 kDa antigen were similar between diseased, infected patients and the uninfected, normal subjects, suggesting that it may be stimulated as a cross-reactive antigen. Antibody to the 28, 38, and 90 kDa antigens were significantly more common in diseased patients (>90%) versus normal subjects (p<0.01, p<0.002, and p<0.002, respectively) and were unique among diseased, infected patients, which may be indicative of infections with Aa. A 65 kDa antigen showed an increased frequency of reaction in the AP versus the EOP (p= 0.01) patients, which exemplified a potential distinction in response to Aa between adult and early-onset disease classifications. Seventeen of 22 OMA could be detected in every sample from at least one patient. Longitudinal samples from seropositive EOP and AP reacted 80-100% of the time with the 17, 28, and 100 kDa antigens. Finally, five antigens of 15, 38, 58, 65, and 79 kDa were detected in 33-83% of the seropositive patients; however, antibody to these OMA reacted variably at different sampling points, suggesting some antigenic response diversity over time.

Original languageEnglish (US)
Pages (from-to)732-741
Number of pages10
JournalJournal of Clinical Periodontology
Volume26
Issue number11
StatePublished - Nov 1999

Fingerprint

Aggregatibacter actinomycetemcomitans
Antibody Formation
Antigens
Membranes
Serum
Periodontitis
Antigenic Variation
Antibody Specificity
Host Specificity
Infection
Healthy Volunteers

Keywords

  • A. actinomycetemcomitans
  • Disease activity
  • Outer membrane antigens
  • Serum antibody

ASJC Scopus subject areas

  • Dentistry(all)

Cite this

Longitudinal human serum antibody responses to outer membrane antigens of Actinobacillus actinomycetemcomitans. / Ebersole, Jeffrey L.; Steffen, Michelle J.; Cappelli, David.

In: Journal of Clinical Periodontology, Vol. 26, No. 11, 11.1999, p. 732-741.

Research output: Contribution to journalArticle

Ebersole, Jeffrey L. ; Steffen, Michelle J. ; Cappelli, David. / Longitudinal human serum antibody responses to outer membrane antigens of Actinobacillus actinomycetemcomitans. In: Journal of Clinical Periodontology. 1999 ; Vol. 26, No. 11. pp. 732-741.
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AB - We hypothesize that serum antibody responses to antigens of a periodontopathogen would vary temporally and that the specificity of these host antibodies would relate to infection and disease activity. To test the hypothesis, we obtained between 6 and 13 serum samples from Actinobacillus actinomycetemcomitans (Aa)-positive (serological and microbiological) periodontitis patients at time points between 18 and 42 months into the study, and evaluated specific antibody responses to outer membrane antigens (OMA) of Aa strain Y4. Sera from these patients detected 22 different OMA. Early-onset (EOP; n=7) and adult (AP; n=11) periodontitis patients responded to 35% and 41% of the OMA, respectively. 2 of 9 sera from healthy subjects detected no antigens and 7/9 sera detected 7% of the OMA (p<0.0001 versus EOP and AP). The frequency of antibody responses to the 17 kDa antigen were similar between diseased, infected patients and the uninfected, normal subjects, suggesting that it may be stimulated as a cross-reactive antigen. Antibody to the 28, 38, and 90 kDa antigens were significantly more common in diseased patients (>90%) versus normal subjects (p<0.01, p<0.002, and p<0.002, respectively) and were unique among diseased, infected patients, which may be indicative of infections with Aa. A 65 kDa antigen showed an increased frequency of reaction in the AP versus the EOP (p= 0.01) patients, which exemplified a potential distinction in response to Aa between adult and early-onset disease classifications. Seventeen of 22 OMA could be detected in every sample from at least one patient. Longitudinal samples from seropositive EOP and AP reacted 80-100% of the time with the 17, 28, and 100 kDa antigens. Finally, five antigens of 15, 38, 58, 65, and 79 kDa were detected in 33-83% of the seropositive patients; however, antibody to these OMA reacted variably at different sampling points, suggesting some antigenic response diversity over time.

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