Immune system transcriptome in gingival tissues of young nonhuman primates

• Published in: Journal of periodontal research Vol. 51; no. 2; pp. 152 - 163
• Main Authors: Gonzalez, O. A., Nagarajan, R., Novak, M. J., Orraca, L., Gonzalez-Martinez, J. A., Kirakodu, S. S., Ebersole, J. L.
• Format: Journal Article
• Language: English
• Published: United States Blackwell Publishing Ltd 01-04-2016
• Subjects: aging; Animals; Gingiva; Immune System; inflammation; Macaca mulatta; nonhuman primates; Oligonucleotide Array Sequence Analysis; Periodontitis; Transcriptome; aging; nonhuman primates; inflammation; periodontitis
• ISSN: 0022-3484; 1600-0765
• DOI: 10.1111/jre.12293

Background and Objective
Young/adolescent humans harbor many microorganisms associated with periodontal disease in adults and show substantial gingival inflammatory responses. However, younger individuals do not demonstrate the soft‐ and hard‐tissue destruction that hallmark periodontitis.
Material and Methods
This study evaluated responses to the oral microbial ecology in gingival tissues from clinically healthy young Macaca mulatta (< 3 years of age) compared with older animals (5–23 years of age). RNA was isolated from the tissues and analyzed for the transcriptome using the Rhesus Macaque GeneChip (Affymetrix).
Results
Global transcriptional profiling of four age groups revealed a subset of 159 genes that were differentially expressed across at least one of the age comparisons. Correlation metrics generated a relevance network ion of these genes. Partitioning of the relevance network revealed seven distinct communities comprising functionally related genes associated with host inflammatory and immune responses. A group of genes was identified that were selectively increased/decreased or positively/negatively correlated with gingival profiles in the animals. A principal components analysis created metagenes of expression profiles for classifying the 23 animals.
Conclusion
The results provide novel system‐level insights into gene‐expression differences in gingival tissues from healthy young animals, weighted toward host responses associated with anti‐inflammatory biomolecules or those linked with T‐cell regulation of responses. The combination of the regulated microenvironment may help to explain the apparent ‘resistance’ of younger individuals to developing periodontal disease.