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Liver X receptors contribute to periodontal pathogen‐elicited inflammation and oral bone loss
Author(s) -
Huang N.,
ShaikDasthagirisaheb Y.B.,
LaValley M.P.,
Gibson F.C.
Publication year - 2015
Publication title -
molecular oral microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.18
H-Index - 77
eISSN - 2041-1014
pISSN - 2041-1006
DOI - 10.1111/omi.12103
Subject(s) - porphyromonas gingivalis , liver x receptor , inflammation , immunology , dysbiosis , periodontitis , biology , inflammasome , immune system , innate immune system , tlr2 , nuclear receptor , medicine , gut flora , transcription factor , biochemistry , gene
Summary Periodontal diseases are chronic oral inflammatory diseases that are polymicrobial in nature. The presence of specific bacteria in subgingival plaque such as Porphyromonas gingivalis is associated with microbial dysbiosis and the modulation of host immune response. Bacterially elicited innate immune activation and inflammation are key elements implicated in the destruction of soft and hard tissues supporting the teeth. Liver X receptors ( LXR s) are nuclear hormone receptors with important function in lipid homeostasis, inflammation, and host response to infection; however, their contribution to chronic inflammatory diseases such as periodontal disease is not understood. The aim of this study was to define the contribution of LXR s in the development of immune response to P. gingivalis and to assess the roles that LXR s play in infection‐elicited oral bone loss. Employing macrophages, we observed that P. gingivalis challenge led to reduced LXR α and LXR β gene expression compared with that observed with unchallenged wild‐type cells. Myeloid differentiation primary response gene 88 (MyD88)‐independent, Toll/interleukin‐1 receptor‐domain‐containing adapter‐inducing interferon‐β ( TRIF )‐dependent signaling affected P. gingivalis ‐mediated reduction in LXR α expression, whereas neither pathway influenced the P. gingivalis effect on LXR β expression. Employing LXR agonist and mice deficient in LXR s, we observed functional effects of LXR s in the development of a P. gingivalis ‐elicited cytokine response at the level of the macrophage, and participation of LXR s in P. gingivalis ‐elicited oral bone loss. These findings identify novel importance for LXR s in the pathogenesis of P. gingivalis infection‐elicited inflammation and oral bone loss.