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J Periodontol. 2017 Aug;88(8):e129-e139. doi: 10.1902/jop.2017.160815. Epub 2017 Mar 31.

A Sialidase-Deficient Porphyromonas gingivalis Mutant Strain Induces Less Interleukin-1β and Tumor Necrosis Factor-α in Epi4 Cells Than W83 Strain Through Regulation of c-Jun N-Terminal Kinase Pathway.

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Department of Periodontics, School of Stomatology, China Medical University, Shenyang, Liaoning, China.
Department of Periodontics and Oral Medicine, University of Michigan, Ann Arbor, MI.



Porphyromonas gingivalis is one of the major periodontal pathogens. In a previous study, a mouse abscess model showed that sialidase deficiency of P. gingivalis weakened its virulence, but the mechanism behind this observation remains unknown.


A sialidase-deficient mutant strain (△PG0352) and a complemented strain (com△PG0352) were constructed. Epi4 cells were stimulated by wild-type strain P. gingivalis W83, △PG0352, or com△PG0352. Real-time polymerase chain reaction was carried out to detect expression of virulent genes in P. gingivalis and interleukin (IL)-1β, IL-6, IL-8, and tumor necrosis factor (TNF)-α in epi4 cells. Activities of sialidase, gingipains, and lipopolysaccharide (LPS) were compared among the different P. gingivalis strains. Levels of IL-1β and TNF-α in the epi4 cells supernatant were detected by enzyme-linked immunosorbent assay and levels of p38, extracellular signal-regulated kinase, c-Jun N-terminal kinase (JNK), and phospho-c-Jun were detected by western blotting.


Compared with P. gingivalis W83 and com△PG0352, activities of Kgp and Rgp gingipains and amount of LPS decreased in △PG0352, whereas there were no differences in LPS activity among these three strains. Level of phospho-JNK was lower in epi4 cells stimulated by △PG0352. △pG0352 induced less IL-1β and TNF-α and more IL-8 in epi4 cells; differences in IL-1β and TNF-α could not be detected after JNK blocking.


A sialidase-deficient P. gingivalis mutant strain induces less IL-1β and TNF-α in epi4 cells than W83 strain through regulation of JNK pathway.


Epithelial cells; JNK mitogen-activated protein kinases; Porphyromonas gingivalis; gingiva; neuraminidase

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