Friday, March 23, 2012: 10:45 a.m. - 12:15 p.m.
Presentation Type: Oral Session
Although the prevalence of chronic inflammatory disorders (e.g., periodontal disease) increases with aging, the mechanisms underlying this observation remain incompletely understood. Cytosolic multiprotein complexes that involve members of the NOD-like receptors (NLRs) family (i.e., inflammasomes) are emerging innate immune regulators of inflammation and infection; nevertheless their constitutive expression and age-related changes in gingival tissues remain unclear. Objectives: To determine the expression of inflammasome genes in healthy and periodontitis gingival tissues across the lifespan Methods: Expression analysis of 16 genes involved in inflammasome pathways was performed in gingival biopsies from 20 healthy nonhuman primates (Macaca mulatta) (5/group) distributed in young (<3 yrs), adolescent (3-7 yrs), adult (12-15 yrs) and aged (18-22 yrs) groups, and 10 animals with periodontitis (5 adults and 5 aged), using the GeneChip® Rhesus Macaque Genome Array. Results: Inflammasome-activating NLRs were differentially expressed in healthy gingival tissue, with high expression of NLRP3 and NLRB/NAIP, intermediate expression of NLRPs 1, 2, 6 and 8; and low expression of NLRPs 4, 5, 7, 10, 11, 14, and NLRC4/IPAF. NLRP2 and 14 were over-expressed in aged compared with young healthy gingival tissue. Although caspase-1 expression did not change with age, there were age-related differences in the expression of its substrates pro-IL1β and pro-IL18. Significant reduction in NLRP1 and NLRP2 expression was related to periodontitis in adult and aged gingival tissues respectively. Finally, pro-IL1β, but not pro-IL-18 expression, increased in both aged and adult periodontitis tissues, and caspase-1 was only up-regulated in adult periodontitis tissues. Conclusions: These results suggest that inflammasome genes are expressed in healthy gingival tissue at different levels, and the expression of a subset of these genes appears to change with age and periodontitis. The mechanisms by which these variations could be related to a higher prevalence and/or severity of periodontal disease with aging will require further research.This abstract is based on research that was funded entirely or partially by an outside source: NIH/NCRR 2P20RR020145
Keywords: Aging, Gene expression, Immunology, Inflammation and Periodontal disease