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Treponema denticola enolase contributes to the production of antibodies against ENO1 but not to the progression of periodontitis

Title
Treponema denticola enolase contributes to the production of antibodies against ENO1 but not to the progression of periodontitis
Authors
Lee, AhreumKim, Yong C.Baek, KeumjinAlam, JehanChoi, Yun S.Rheu, YaeeunShin, Yoo JinKim, SungtaeKim, Hyun-DuckSong, Yeong W.Choi, Youngnim
Ewha Authors
한인식
SCOPUS Author ID
한인식scopus
Issue Date
2018
Journal Title
VIRULENCE
ISSN
2150-5594JCR Link

2150-5608JCR Link
Citation
VIRULENCE vol. 9, no. 1, pp. 1263 - 1272
Keywords
Treponema denticolaenolaseperiodontitisautoantibodyTNF alpha
Publisher
TAYLOR &

FRANCIS INC
Indexed
SCIE; SCOPUS WOS scopus
Document Type
Article
Abstract
Autoantibodies against alpha-enolase (ENO1) are often detected in various infectious and autoimmune diseases. Anti-ENO1 antibody titers were reported to be associated with the severity of periodontitis in patients with rheumatoid arthritis. Because the enolase of the periodontal pathogen Treponema denticola (TdEno) has the highest homology with ENO1 among the enolases of human-associated bacteria, we hypothesized that anti-ENO1 autoantibodies produced during the immune response to TdEno may contribute to the progression of periodontitis and tested it in human and mouse systems. In human subjects with healthy periodontium or chronic periodontitis, a strong positive correlation between the levels of anti-TdEno and anti-ENO1 antibodies was observed. In addition, the purified anti-TdEno antibodies recognized ENO1 as well as TdEno in a dot blot, confirming the cross-reactivity between TdEno and ENO1. However, anti-ENO1 antibody titers were not associated with the severity of periodontitis. To further investigate the role of TdEno in the production of anti-ENO1 antibodies and the progression of periodontitis, mice received an oral gavage of P. gingivalis alone, subcutaneous immunization with TdEno alone, or both P. gingivalis oral gavage and TdEno immunization. Immunization with TdEno induced not only anti-TdEno but also anti-mouse Eno1 (mEno1) antibodies and increased the expression of TNF in the gingival tissues. However, alveolar bone loss was not increased by TdEno immunization. In conclusion, autoreactive anti-ENO1/mEno1 antibodies that are produced as byproducts during the antibody response to TdEno play a minimal role in the progression of periodontitis in the absence of rheumatoid arthritis.
DOI
10.1080/21505594.2018.1496775
Appears in Collections:
사범대학 > 과학교육과 > Journal papers
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