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KMID : 0620920180500030013
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Experimental & Molecular Medicine
2018 Volume.50 No. 3 p.13 ~ p.13
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Interrupting oral infection of Porphyromonas gingivalis with anti-FimA antibody attenuates bacterial dissemination to the arthritic joint and improves experimental arthritis
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Jeong Sang-Hoon
Nam Yoo-Jun
Jung Hye-Rin
Kim Ju-Ryun
Rim Ye-Ri Alice
Park Na-Rae
Lee Ki-Jun
Choi Seung-Jin
Jang Yeon-Sue
Kim Ye-Na
Moon Ji-Hoi
Jung Seung-Min
Park Sung-Hwan
Ju Ji-Hyeon
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Abstract
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Rheumatoid arthritis (RA) is a chronic autoimmune disease that typically results in strong inflammation and bone destruction in the joints. It is generally known that the pathogenesis of RA is linked to cardiovascular and periodontal diseases. Though rheumatoid arthritis and periodontitis share many pathologic features such as a perpetual inflammation and bone destruction, the precise mechanism underlying a link between these two diseases has not been fully elucidated. Collagen-induced arthritis (CIA) mice were orally infected with Porphyromonas gingivalis (Pg) or Pg preincubated with an anti-FimA antibody (FimA Ab) specific for fimbriae that are flexible appendages on the cell surface. Pg-infected CIA mice showed oral microbiota disruption and increased alveolar bone loss and had synovitis and joint bone destruction. However, preincubation with FimA Ab led to a significant reduction in the severity of both oral disease and arthritis. Moreover, FimA Ab attenuated bacterial attachment and aggregation on human gingival and rheumatoid arthritis synovial fibroblasts. In addition, we discovered bacteria may utilize dendritic cells, macrophages and neutrophils to migrate into the joints of CIA mice. These results suggest that disrupting Pg fimbriae function by FimA Ab ameliorates RA.
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KEYWORD
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Rheumatoid arthritis
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