Modulation of proinflammatory mediators by viruses-bacteria synergism in human osteoblasts-an in vitro study.

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 E (PGE) from osteoblasts were determined. The effects of povidone-iodine (PVP-I) on the secretion of IL-6 and PGE were also examined.

Methods: Viability of treated osteoblastic cells (MG63) was examined by detection the mitochondrial dehydrogenase activity. Secretion of IL-6 and PGE 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 PGE in MG63 cells. The additive/synergistic effects of Pg-LPS/poly I:C on production of IL-6 and PGE 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 PGE 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.