Background. Proinflammatory and anti-inflammatory cytokines play a key role in the pathogenesis of periodontal diseases. Secretion of bioactive IL-35 has been described by T regulatory cells ( ) and is required for their maximal suppressive activity. are involved in the modulation of local immune response in chronic periodontitis patients. Objective. Hence, the present study was aimed to investigate the expression of IL-35 mRNA in chronic periodontitis and aggressive periodontitis patients. Materials and Methods. The present study was carried out in 60 subjects, which included 20 chronic periodontitis patients, 20 aggressive periodontitis patients, and 20 periodontally healthy controls. IL-35 mRNA expression in gingival tissue samples of all subjects was semiquantitatively analyzed using Reverse Transcriptase Polymerase Chain Reaction (RT-PCR). Results. The present study demonstrated the expression of IL-35 mRNA in gingival tissues of all the three groups. IL-35 mRNA expression was highest in chronic periodontitis subjects ( ) as compared to the aggressive periodontitis group ( ) and least seen in healthy patients ( ). Conclusion. The increased expression of IL-35 in chronic and aggressive periodontitis suggests its possible role in pathogenesis of periodontitis. Future studies done on large samples with intervention will strengthen our result. 1. Introduction Periodontal diseases are considered to be multifactorial diseases, where putative periodontopathogens trigger inflammatory and immune responses. It is characterized by irreversible loss of alveolar bone and connective tissue attachment in the periodontium which ultimately results in the loss of teeth. These pathogens are known to produce proteolytic enzymes as well as elicit signals in resident gingival cells or in immune cells infiltrating the gingival tissues that result in immune responses; these responses lead to either the successful removal of the pathogens or to host mediated destruction of the periodontal tissues [1]. Gingival inflammation is regulated by reciprocal interactions between various cell types including, leukocytes, epithelial cells, fibroblasts, and endothelial cells. Among the many immune and inflammatory mediators known cytokines have attracted special attention. Proinflammatory and anti-inflammatory cytokines play a key role in the pathogenesis of periodontal disease thereby influencing destruction, remodeling, and repair of periodontal tissues [2]. Interleukin-12 (IL-12) is one such cytokine which appears to contribute to inflammatory response in numerous physiological and
References
[1]
A. Orozco, E. Gemmell, M. Bickel, and G. J. Seymour, “Interleukin-1β, interleukin-12 and interleukin-18 levels in gingival fluid and serum of patients with gingivitis and periodontitis,” Oral Microbiology and Immunology, vol. 21, no. 4, pp. 256–260, 2006.
[2]
L. I. Holla, A. Fassmann, A. Stejskalová, V. Znojil, J. Van？ek, and J. Vacha, “Analysis of the interleukin-6 gene promoter polymorphisms in Czech patients with chronic periodontitis,” Journal of Periodontology, vol. 75, no. 1, pp. 30–36, 2004.
[3]
Z. Ning-Wei, “Interleukin (IL)-35 is raising our expectations,” Revista Medica de Chile, vol. 138, no. 6, pp. 758–766, 2010.
[4]
L. W. Collison and D. A. A. Vignali, “Interleukin-35: odd one out or part of the family?” Immunological Reviews, vol. 226, no. 1, pp. 248–262, 2008.
[5]
W. Niedbala, X.-Q. Wei, B. Cai et al., “IL-35 is a novel cytokine with therapeutic effects against collagen-induced arthritis through the expansion of regulatory T cells and suppression of Th17 cells,” European Journal of Immunology, vol. 37, no. 11, pp. 3021–3029, 2007.
[6]
C. R. Cardoso, G. P. Garlet, A. P. Moreira, W. Martins Jr., M. A. Rossi, and J. S. Silva, “Characterization of CD4+CD25+ natural regulatory T cells in the inflammatory infiltrate of human chronic periodontitis,” Journal of Leukocyte Biology, vol. 84, no. 1, pp. 311–318, 2008.
[7]
D. F. Kinane and T. C. Hart, “Genes and gene polymorphisms associated with periodontal disease,” Critical Reviews in Oral Biology and Medicine, vol. 14, no. 6, pp. 430–449, 2003.
[8]
Y. Matsuki, T. Yamamoto, and K. Hara, “Localization of interleukin-1 (IL-1) mRNA-expressing macrophages in human inflamed gingiva and IL-1 activity in gingival crevicular fluid,” Journal of Periodontal Research, vol. 28, no. 1, pp. 35–42, 1993.
[9]
A. I. Dongari-Bagtzoglou and J. L. Ebersole, “Increased presence of interleukin-6 (IL-6) and IL-8 secreting fibroblast subpopulations in adult periodontitis,” Journal of Periodontology, vol. 69, no. 8, pp. 899–910, 1998.
[10]
L. W. Collison, C. J. Workman, T. T. Kuo et al., “The inhibitory cytokine IL-35 contributes to regulatory T-cell function,” Nature, vol. 450, no. 7169, pp. 566–569, 2007.
[11]
T. Nakajima, K. Ueki-Maruyama, T. Oda et al., “Regulatory T-cells infiltrate periodontal disease tissues,” Journal of Dental Research, vol. 84, no. 7, pp. 639–643, 2005.
[12]
N. Dutzan, J. Gamonal, A. Silva, M. Sanz, and R. Vernal, “Over-expression of forkhead box P3 and its association with receptor activator of nuclear factor-κ B ligand, interleukin (IL) -17, IL-10 and transforming growth factor-β during the progression of chronic periodontitis,” Journal of Clinical Periodontology, vol. 36, no. 5, pp. 396–403, 2009.
[13]
S. A. Joosten and T. H. M. Ottenhoff, “Human CD4 and CD8 regulatory T cells in infectious diseases and vaccination,” Human Immunology, vol. 69, no. 11, pp. 760–770, 2008.
[14]
T. Aoyagi, K. Yamazaki, Y. Kabasawa-Katoh et al., “Elevated CTLA-4 expression on CD4 T cells from periodontitis patients stimulated with Porphyromonas gingivalis outer membrane antigen,” Clinical and Experimental Immunology, vol. 119, no. 2, pp. 280–286, 2000.
[15]
N. Silva, N. Dutzan, M. Hernandez et al., “Characterization of progressive periodontal lesions in chronic periodontitis patients: levels of chemokines, cytokines, matrix metalloproteinase-13, periodontal pathogens and inflammatory cells,” Journal of Clinical Periodontology, vol. 35, no. 3, pp. 206–214, 2008.
[16]
Y. Belkaid and B. T. Rouse, “Natural regulatory T cells in infectious disease,” Nature Immunology, vol. 6, no. 4, pp. 353–360, 2005.
[17]
V. Chaturvedi, L. W. Collison, C. S. Guy, C. J. Workman, and D. A. A. Vignali, “Cutting edge: human regulatory T cells require IL-35 to mediate suppression and infectious tolerance,” Journal of Immunology, vol. 186, no. 12, pp. 6661–6666, 2011.
[18]
C. W. O. Ernst, J. E. Lee, T. Nakanishi et al., “Diminished forkhead box P3/CD25 double-positive T regulatory cells are associated with the increased nuclear factor-kB ligand (RANKL+) T cells in bone resorption lesion of periodontal disease,” Clinical and Experimental Immunology, vol. 148, no. 2, pp. 271–280, 2007.
[19]
E. Bardel, F. Larousserie, P. Charlot-Rabiega, A. Coulomb-L'Herminé, and O. Devergne, “Human CD4+CD25+Foxp3+ regulatory T cells do not constitutively express IL-35,” Journal of Immunology, vol. 181, no. 10, pp. 6898–6905, 2008.
