Abstract
Evidence has shown activation of T and B cells in gingival tissues in experimental models and in humans diagnosed with periodontitis. The results of this adaptive immune response are noted both locally and systemically with antigenic specificity for an array of oral bacteria, including periodontopathic species, e.g., Porphyromonas gingivalis and Aggregatibacter actinomycetemcomitans. It has been recognized through epidemiological studies and clinical observations that the prevalence of periodontitis increases with age. This report describes our studies evaluating gingival tissue transcriptomes in humans and specifically exploiting the use of a non-human primate model of naturally occurring periodontitis to delineate gingival mucosal tissue gene expression profiles focusing on cells/genes critical for the development of humoral adaptive immune responses. Patterns of B cell and plasmacyte genes were altered in aging healthy gingival tissues. Substantial increases in a large number of genes reflecting antigen-dependent activation, B cell activation, B cell proliferation, and B cell differentiation/maturation were observed in periodontitis in adults and aged animals. Finally, evaluation of the relationship of these gene expression patterns with those of various tissue destructive molecules (MMP2, MMP9, CTSK, TNFα, and RANKL) showed a greater frequency of positive correlations in healthy tissues versus periodontitis tissues, with only MMP9 correlations similar between the two tissue types. These results are consistent with B cell response activities in healthy tissues potentially contributing to muting the effects of the tissue destructive biomolecules, whereas with periodontitis this relationship is adversely affected and enabling a progression of tissue destructive events.
Highlights
“Negative, age-related changes in our innate and adaptive immune systems are known collectively as immunosenescence
A protocol approved by the Institutional Animal Care and Use Committee (IACUC) of the University of Puerto Rico, enabled anesthetized animals to be examined for clinical measures of periodontal health, including probing pocket depth (PPD), and bleeding on probing (BOP) as we have described previously [49]
Since host-induced tissue destruction is a feature of the chronic inflammation of periodontitis, we explored the relationship between gingival expression of the B cell/plasmacyte group of genes and expression of genes associated with periodontal tissue destruction during health and periodontal disease irrespective of age
Summary
“Negative, age-related changes in our innate and adaptive immune systems are known collectively as immunosenescence. Aging is a degenerative process with hallmarks of chronic inflammation and oxidative stressrelated mitochondrial damage that contribute to the initiation of other deleterious processes within cells, including epigenetic modification of gene expression that can affect normal cellular functions [1] Alterations in both innate and adaptive immunity have been universally observed in aging populations and have led to the birth of such terms as “immune-aging” or “immunosenescence” to reflect the deteriorating nature of the immune system [2]. Recent studies are showing that the coincident loss of normal innate and adaptive immune response capacity with aging, combined with low-grade chronic inflammation, work together to effectively alter immunocompetence and promote the pathogenesis of a diverse number of diseases [6] These findings suggest that “unhealthy” aging is driven in part by the dysregulation of immunoactivation [7]. We spotlight in this report on cellular markers of humoral adaptive immunity related to aging and chronic inflammatory disease of the oral mucosa and alveolar bone
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