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Published on: January 27, 2023
Modulation of proinflammatory mediators by viruses-bacteria synergism in human osteoblasts-an in vitro study
Ya-Yun Lee1, Ming-Ju Li2, Zhu-Yun Yu2
1Institute of Oral Biology, National Yang Ming Chiao Tung University, Taipei, Taiwan; Department of Dentistry, National Yang Ming Chiao Tung University, Taipei, Taiwan; Department of Stomatology, Taipei Veterans General Hospital, Taipei, Taiwan.
Background/Purpose:
Viruses-bacteria synergistic interaction is associated with destructive periodontal diseases. However, the underlying mechanism for tissue destruction is not fully elucidated. In this study, lipopolysaccharide from Porphyromonas gingivalis (Pg-LPS) and polyinosinic-polycytidylic acid (poly I:C) were used to simulate bacteria and viruses, respectively. The possible combined effects of both molecular patterns on secretion of interleukin (IL)-6 and prostaglandin E2 (PGE2) from osteoblasts were determined. The effects of povidone-iodine (PVP-I) on the secretion of IL-6 and PGE2 were also examined.
Methods:
Viability of treated osteoblastic cells (MG63) was examined by detection the mitochondrial dehydrogenase activity. Secretion of IL-6 and PGE2 was detected using the enzyme-linked immunosorbent assay (ELISA). Mitogen-activated protein kinases (MAPKs) and cyclooxygenase-2 (COX-2) were determined using the Western blotting analysis.
Results:
Pg-LPS or poly I:C significantly enhanced the production of IL-6 and PGE2 in MG63 cells. The additive/synergistic effects of Pg-LPS/poly I:C on production of IL-6 and PGE2 were evident. The levels of phosphorylation of p38 MAPK and c-Jun N-terminal kinase (JNK) and expression of COX-2 protein were enhanced by Pg-LPS and/or poly I:C. On the other hand, the level of phosphorylation of extracellular signal-regulated kinase (ERK) was reduced by Pg-LPS and/or poly I:C. The stimulatory secretion of PGE2 by poly I:C was significantly reduced by PVP-I.
Conclusion:
Concomitant infection of viruses and bacteria may be potentially harmful to the tooth supporting tissues by production of proinflammatory mediators. The results suggest the potential anti-inflammatory effect of PVP-I on bacterial or viral infection.
Insights
Combined bacterial and viral infections increase inflammatory mediators, potentially harming tooth tissues. Povidone-iodine (PVP-I) shows anti-inflammatory effects against these infections.
Area of Science:
- Oral biology
- Immunology
- Periodontology
Background:
- Synergistic interactions between viruses and bacteria are implicated in destructive periodontal diseases.
- The precise mechanisms driving tissue destruction in these conditions remain incompletely understood.
- This study utilizes Porphyromonas gingivalis lipopolysaccharide (Pg-LPS) and polyinosinic-polycytidylic acid (poly I:C) as surrogates for bacterial and viral pathogens, respectively.
Purpose of the Study:
- To investigate the combined effects of Pg-LPS and poly I:C on the secretion of interleukin-6 (IL-6) and prostaglandin E2 (PGE2) by osteoblasts.
- To evaluate the potential anti-inflammatory impact of povidone-iodine (PVP-I) on IL-6 and PGE2 secretion induced by these pathogens.
Main Methods:
- Osteoblastic cells (MG63) were treated with Pg-LPS and/or poly I:C.
- Cell viability was assessed using mitochondrial dehydrogenase activity assays.
- Secretion of IL-6 and PGE2 was quantified via enzyme-linked immunosorbent assay (ELISA).
- Mitogen-activated protein kinases (MAPKs) and cyclooxygenase-2 (COX-2) were analyzed using Western blotting.
Main Results:
- Both Pg-LPS and poly I:C significantly increased IL-6 and PGE2 production in MG63 cells, with additive or synergistic effects observed when used together.
- Pg-LPS and/or poly I:C enhanced the phosphorylation of p38 MAPK and JNK, and increased COX-2 expression.
- Extracellular signal-regulated kinase (ERK) phosphorylation was reduced by Pg-LPS and/or poly I:C.
- PVP-I significantly inhibited poly I:C-induced PGE2 secretion.
Conclusions:
- Concomitant viral and bacterial infections may exacerbate tooth-supporting tissue damage through the production of pro-inflammatory mediators.
- The findings suggest a potential therapeutic role for PVP-I in mitigating inflammation associated with bacterial or viral infections.
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