Role of interleukin-17 signaling in acute periodontal disease
Yu, Jeffrey John
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The immune system is a diverse body of highly mobile hematopoetic cells and fixed resident cells. These cells act to protect the host from pathogens and coordinate an effective response through cytokines. An overactive and extended response results in inflammatory pathology, whereas a less robust response results in infection or a failure to eliminate tumors. Interleukin-17 (IL-17) is a pleiotropic cytokine implicated in inflammatory pathology as seen in rheumatoid arthritis, but is essential to protect the host from pathogens susceptible to neutrophil-mediated immunity. Periodontal disease is a chronic disease that requires bacterial invasion but results in inflammatory pathology such as periodontal bone destruction which is mediated by an extended immune response. We used mice defective for IL-17 signaling (IL-17RA KO mice) in a murine model of periodontal disease and found that such mice were more susceptible to periodontal bone loss due to a failure to recruit neutrophils to infected tissues. Interestingly, female IL-17RA KO mice were more susceptible to bone loss than males and were unable to upregulate neutrophil recruitment proteins, whereas male IL-17RA KO mice failed to increase neutrophil growth factors. The distribution of disease outcomes between genders illustrates an unexpected concern that may come from inflammatory cytokine inhibition, particularly in women.