Abstract
High mobility group box 1 (HMGB1), a nonhistone DNA-binding protein, is released into the extracellular space and promotes inflammation. HMGB1 binds to related cell signaling transduction receptors, including receptor for advanced glycation end products (RAGE), which actively participate in vascular and inflammatory diseases. The aim of this study was to examine whether RAGE and HMGB1 are involved in the pathogenesis of pulpitis and investigate the effect of Prevotella intermedia (P. intermedia) lipopolysaccharide (LPS) on RAGE and HMGB1 expression in odontoblast-like cells (OLC-1). RAGE and HMGB1 expression levels in clinically inflamed dental pulp were higher than those in healthy dental pulp. Upregulated expression of RAGE was observed in odontoblasts, stromal pulp fibroblasts-like cells, and endothelial-like cell lining human pulpitis tissue. Strong cytoplasmic HMGB1 immunoreactivity was noted in odontoblasts, whereas nuclear HMGB1 immunoreactivity was seen in stromal pulp fibroblasts-like cells in human pulpitis tissue. LPS stimulated OLC-1 cells produced HMGB1 in a dose-dependent manner through RAGE. HMGB1 translocation towards the cytoplasm and secretion from OLC-1 in response to LPS was inhibited by TPCA-1, an inhibitor of NF-κB activation. These findings suggest that RAGE and HMGB1 play an important role in the pulpal immune response to oral bacterial infection.
Highlights
Dental caries and subsequent tooth pulp inflammation are major oral health issues caused by oral bacterial infection
Western blot analysis of 4 samples pooled from 15 different pulpitis patients or 3 samples pooled from 15 healthy tissues were probed using a specific anti-receptor for advanced glycation end products (RAGE) Ab (Figure 1(b))
A strong RAGE signal was found in the pulpitis tissues, whereas weak protein signal was seen in the healthy tissue extracts
Summary
Dental caries and subsequent tooth pulp inflammation (pulpitis) are major oral health issues caused by oral bacterial infection. Apart from a rich neurovascular supply, the pulp cavity is home to odontoblasts (the cells that form dentin in the tooth) which are involved in innate immunity against dentin-invading pathogens and are the first to encounter the caries bacterial antigens. It can induce dental pulp fibroblasts to release IL-6 [7] and IL-8 [8] in vitro These cytokines have previously been implicated in the pathogenesis of pulpitis [9,10,11]. While monocytes or fibroblasts in dental pulp tissues have been found to express proinflammatory cytokines, it is not clear whether odontoblasts are involved in the host response and/or produce inflammatory mediators upon stimulation with LPS from P. intermedia
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