歯髄炎の病態形成におけるInterferon-γ inducible protein 10(IP-10)の役割

Dental pulp tissue surrounded by the hard tissue lacks epithelium lining and is in the special environment without the collateral circulatory system. For these specific anatomical characteristics, it is considered that the pulp tissue is easily led to irreversible pulpitis once this tissue is subjected to bacterial irritants. Therefore, to clarify the pathogenesis of pulpitis may lead to the development of new therapeutic approach to control this inflammation and improve the chance of spontaneous healing. The pulpitis is characterized as the immune response which is mainly triggered by invasion of the cariesrelated microorganisms into dental tubules and pulp. In this inflammation progresses, the significant inflammatory cells predominantly comprised of memory T cells and activated T cells infiltrates and recruitments into the lesion. However, these inflammatory infiltration mechanisms are far from being understood. Recently, it has been demonstrated that interferon-gamma-inducible protein-10 (IP-10), one of chemokines, have chemotactic activities against lymphocytes, binds to CXCR3 and then involves in the chemotaxis of CXCR3-positive activated T cells. It is conceivable that IP-10 may have an important regulatory role in activated T cell migration into inflamed tissue. Then, the purpose of this study is to elucidate the role of IP-10-CXCR3 system in the pathogenesis of pulpitis. First, in RT-PCR the expression levels of IP-10 mRNA in clinically inflamed pulp tissues were significantly increased than those in normal pulp tissue. Immunostaining results revealed that IP-10 was observed on fibroblasts, macrophages and endothelial cells in inflamed pulp tissue and CXCR3 was observed on lymphocytes migrated into pulp tissue. Second, the pulp fibroblast-like cells derived from normal dental pulp and PMA-differentiated human monocytic cell line (THP-1 cells) were stimulated with lived bacteria (Streptocossus mutans and Lactobacillus plantarum, which were reported to exist predominatly in dental caries lesions), lipoteichoic acids, peptideglycans, or various inflammatory cytokines in vitro. The result showed that IP-10 was secreted from cultured pulp fibroblasts and THP-1 cells, and that heat-killed S. mutans and L. plantarum did not induce IP-10 secretion. Taken together, this study suggests that the IP-10-CXCR3 system may play an important role in the immune response against the invasion of caries-related bacteria into dental pulp tissue beneath the carious lesion and may be involved in the progression of irreversible pulpitis.

公開日:2010年1月24日で登録したコンテンツは、国立情報学研究所において電子化したものです。