Objective: To determine whether manipulating the actions of NPY, norepinephrine, or IL-1β modulates proinflammatory cytokine gene expression during P. gingivalis-induced inflammation.
Methods: IL-1 Receptor Type I (IL-1RI) knockout mice or wild-type mice administered Y1R antagonist or α- and β -AR agonists and antagonists were injected with live P. gingivalis or vehicle into tissues over the calvaria. After 1 or 3 days, the tissues were processed for quantitative PCR and gene expression was determined for IL-1β, IL-6, and TNF-α.
Results: Gene expression of proinflammatory cytokines was potentiated with the blockade of Y1Rs or both central and peripheral β2-ARs, while antagonizing peripheral β-ARs alone decreased expression. Agonizing α1- or β2-ARs, or antagonizing β1-ARs resulted in decreased expression. Non-specifically antagonizing α-ARs also resulted in decreased expression pointing to a role for α2-ARs in this inflammation model.
Conclusion: Taken together these data suggest that during P. gingivalis-induced inflammation IL-1RI receptors are necessary for proinflammatory cytokine expression (IL-6 and TNF-α) and that the Y1Rs and ARs regulate proinflammatory gene expression with the central β2-adrenergic receptors playing a critical role in this regulation. Since NPY, IL-1β, and norepinephrine have been implicated in the stress response, exploring these mechanisms will not only aid in identifying novel therapeutic targets, but elucidate the connection of stress to periodontitis.
Keywords: Bacterial, Gene expression, Immunology, Periodontal disease and Stress
See more of: Periodontal Research - Pathogenesis