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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.

Author information

1
Department of Periodontics, School of Stomatology, China Medical University, Shenyang, Liaoning, China.
2
Department of Periodontics and Oral Medicine, University of Michigan, Ann Arbor, MI.

Abstract

BACKGROUND:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSION:

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.

KEYWORDS:

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

PMID:
28362225
DOI:
10.1902/jop.2017.160815
[Indexed for MEDLINE]
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