Abstract

Periodontal disease is composed of complex disease entities with etiological components comprising complex microorganisms,1,2 with their complex antigenic components. Diverse immunological mechanisms and immune recognition of antigen in periodontal diseases3 render the immune responses not necessarily beneficial to host inherent from the cross-reactivity, ecological commensalisms or antagonisms4,5. These bacteria may include, but not limited to, Porphyromonas gingivalis, Actinobacillus actinomycetemcomitans, Prevotella intermedia, Treponema denticola, Bacteroides forsythus, Campylobacter rectus and Fusobacterium nucleatum1. HSP 60 has been found to be a common antigen of many bacterial pathogens6 and its cross-reactivity were reported7. HSP genes have been cloned in P. gingivalis8, A. actinomycetemcomitans9, B. forsythus10, T. denticola11, F. nucleatum12, C. rectus13, and P. intermedia14. HSPs have also been suggested to be strongly associated with autoimmune destructive mechanism in periodontal disease15-17 and atherosclerosis18 due to bacterial HSP sequence shares a moderate level of sequence homology with mammalian counterpart. We have selected HSP as a candidate antigen for investigating antibody response due to the following important reasons; 1) HSP can be found in all of the selected principal periodontopathogenic organisms, 2) HSP-mediated autoimmune mechanism is being characterized both in periodontal disease and atherosclerosis, thus study of HSP may lead to valuable information, 3) GroEL or DnaK genes has been extensively cloned in periodontopathogenic bacteria. Among HSPs from several periodontopathogenic bacteria, we have selected P. gingivalis HSP due to the following reasons; 1) P. gingivalis has been the most important key pathogen in destructive periodontal diseases2, 2) we have been concentrating on establishment of P. gingivalis HSP-specific T cell lines in periodontal and atherosclerosis patients, 3) HSP from such as F. nucleatum is more likely to be

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