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Protective role of osteopontin in endodontic infection
Author(s) -
Rittling Susan R.,
Zetterberg Craig,
Yagiz Kader,
Skinner Stephen,
Suzuki Noriyuki,
Fujimura Akira,
Sasaki Hajime
Publication year - 2010
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/j.1365-2567.2009.03159.x
Subject(s) - osteopontin , immunology , biology , inflammation , immune system , rankl , acquired immune system , innate immune system , receptor , biochemistry , activator (genetics)
Summary Endodontic infections are polymicrobial infections resulting in bone destruction and tooth loss. The host response to these infections is complex, including both innate and adaptive mechanisms. Osteopontin (OPN), a secreted, integrin‐binding protein, functions in the regulation of immune responses and enhancement of leucocyte migration. We have assessed the role of OPN in the host response to endodontic infection using a well‐characterized mouse model. Periapical bone loss associated with endodontic infection was significantly more severe in OPN‐deficient mice compared with wild‐type 3 weeks after infection, and was associated with increased areas of inflammation. Expression of cytokines associated with bone loss, interleukin‐1α (IL‐1α) and RANKL, was increased 3 days after infection. There was little effect of OPN deficiency on the adaptive immune response to these infections, as there was no effect of genotype on the ratio of bacteria‐specific immunoglobulin G1 and G2a in the serum of infected mice. Furthermore, there was no difference in the expression of cytokines associated with T helper type 1/type2 balance: IL‐12, IL‐10 and interferon‐γ. In infected tissues, neutrophil infiltration into the lesion area was slightly increased in OPN‐deficient animals 3 days after infection: this was confirmed by a significant increase in expression of neutrophil elastase in OPN‐deficient samples at this time‐point. We conclude that OPN has a protective effect on polymicrobial infection, at least partially because of alterations in phagocyte recruitment and/or persistence at the sites of infection, and that this molecule has a potential therapeutic role in polymicrobial infections.