medigraphic.com
ISSN 2007-4360 (Print)
Asociación Mexicana de Periodontología, Colegio de Periodoncistas A.C

2017, Number 1

<< Back Next >>

Rev Mex Periodontol 2017; 8 (1)

Determination of levels of IL-23 soluble receptor in serum and plasma of patients with chronic and aggressive periodontitis

Rivadeneyra-Burgos C, Rodríguez-Montaño R, Ruíz-Gutiérrez AC, Martínez-Rodríguez VC, Meléndez-Ruiz JL, Pita-López ML, Alcázar-Ríos JA, Guerrero-Velázquez C

Language: Spanish
References: 30
Page: 5-10
PDF size: 327.42 Kb.


ABSTRACT

Periodontitis is a chronic immunologic-inflammatory disease primarily caused by Aggregatibacter actinomycetemcomitans and Porphyromonas gingivalis. The most common types of periodontal disease are: chronic (CP) and aggressive (AP) which are characterized by gingival inflammation, formation of periodontal pockets, and loss of insertion and destruction of alveolar bone. However, attachment loss and tissue destruction is faster in AP than CP. Dendritic cells are stimulated by periodontopathogenic bacterias and produce IL-23; this cytokine binds to its specific receptor (IL-23R) trough Th17 cells to induce production of IL-17. It is to be noted that IL-23R can be cleaved and remain as a soluble receptor (IL-23Rs). IL-23 and IL-17 and its receptors indirectly participate in alveolar bone resorption. In this sense, it was found that IL-17 is elevated in patients with CP compared to healthy subjects (HS). However, little has been said about IL-23 and its receptor in periodontitis. Objective: Type of study: descriptive, cross-sectional and analytical. Measuring IL-23Rs levels in serum and plasma of patients with PC, PA and healthy subjects. Material and methods: Serum and plasma were collected from patients with CP (n = 8) and AP (n = 8) as well as from HS (n = 8). The concentration of IL-23Rs was determined by ELISA. Results: There were no significant differences in IL-23Rs between patients with PA and PC compared with SS. However, we found a significant increase in IL-23Rs in the plasma of patients with AP compared to SS. Likewise, we observed a significant increase in PC patients compared with SS. Conclusions: There is an increase in plasma IL-23Rs in patients with PC and PA compared to SS. However, we found no significant differences in serum IL-23Rs between the PC, PA and SS groups.


REFERENCES

  1. Petersen PE, Ogawa H. Strengthening the prevention of periodontal disease: the WHO approach. J Periodontol. 2005; 76 (12): 2187-3193.

  2. Craig RG, Pernat AM, Pecoits-Filho R, Levin NW, Kotanko P. Periodontal diseases and systemic inflammation. Seminars in Dialysis. 2013; 26: 16-39.

  3. Armitage GC. Development of a classification system for periodontal diseases and conditions. Annals of periodontology. Ann Periodontol. 1999; 4 (1): 1-6.

  4. Lindhe J, Karring T, Lang NP. Clinical periodontology and implant dentistry. 4th ed. Oxford, UK ; Malden, MA: Blackwell; 2003; XXIV: p. 1044.

  5. Pihlstrom BL, Michalowicz BS, Johnson NW. Periodontal diseases. Lancet. 2005; 366 (9499): 1809-1820.

  6. Harrington LE, Hatton RD, Mangan PR, Turner H, Murphy TL, Murphy KM et al. Interleukin 17-producing CD4+ effector T cells develop via a lineage distinct from the T helper type 1 and 2 lineages. Nature Immunology. 2005; 6 (11): 1123-1132.

  7. Abdi K, Singh NJ, Spooner E, Kessler BM, Radaev S, Lantz L et al. Free IL-12p40 monomer is a polyfunctional adaptor for generating novel IL-12-like heterodimers extracellularly. J Immunol. 2014; 92 (12): 6028-6036.

  8. Kan SH, Mancini G, Gallagher G. Identification and characterization of multiple splice forms of the human interleukin-23 receptor alpha chain in mitogen-activated leukocytes. Genes Immun. 2008; 9 (7): 631-639.

  9. Franke M, Schroder J, Monhasery N, Ackfeld T, Hummel TM, Rabe B et al. Human and Murine Interleukin 23 Receptors Are Novel Substrates for A Disintegrin and Metalloproteases ADAM10 and ADAM17. J Biol Chem. 2016; 91 (20): 10551-1061.

  10. Yang XP, Ghoreschi K, Steward-Tharp SM, Rodriguez-Canales J, Zhu J, Grainger JR et al. Opposing regulation of the locus encoding IL-17 through direct, reciprocal actions of STAT3 and STAT5. Nature immunology. 2011; 12 (3): 247-254.

  11. Ghoreschi K, Laurence A, Yang XP, Tato CM, McGeachy MJ, Konkel JE et al. Generation of pathogenic T(H)17 cells in the absence of TGF-beta signalling. Nature. 2010; 467 (7318): 967-971.

  12. Bettelli E, Korn T, Kuchroo VK. Th17: the third member of the effector T cell trilogy. Curr Opin Immunol. 2007; 19 (6): 652-657.

  13. Hajishengallis G. Immunomicrobial pathogenesis of periodontitis: keystones, pathobionts, and host response. Trends Immunol. 2014; 35 (1): 3-11.

  14. Ruggeri RM, Saitta S, Cristani M, Giovinazzo S, Tigano V, Trimarchi F et al. Serum interleukin-23 (IL-23) is increased in Hashimoto’s thyroiditis. Endocr J. 2014; 61 (4): 359-363.

  15. Yilmaz SB, Cicek N, Coskun M, Yegin O, Alpsoy E. Serum and tissue levels of IL-17 in different clinical subtypes of psoriasis. Arch Dermatol Res. 2012; 304 (6): 465-469.

  16. Przepiera-Będzak H, Fischer K, Brzosko M. Serum IL-6 and IL-23 Levels and Their Correlation with Angiogenic Cytokines and Disease Activity in Ankylosing Spondylitis, Psoriatic Arthritis, and SAPHO Syndrome. Mediators Inflamm. 2015; 2015: 785705.

  17. Xia LP, Li BF, Shen H, Lu J. Interleukin-27 and interleukin-23 in patients with systemic lupus erythematosus: possible role in lupus nephritis. Scand J Rheumatol. 2015; 4(3):200-5.

  18. van Baarsen LG, Lebre MC, van der Coelen D, Aarrass S, Tang MW, Ramwadhdoebe TH et al. Heterogeneous expression pattern of interleukin 17A (IL-17A), IL-17F and their receptors in synovium of rheumatoid arthritis, psoriatic arthritis and osteoarthritis: possible explanation for nonresponse to anti-IL-17 therapy? Arthritis Res Ther. 2014; 16 (4): 426.

  19. Gumus P, Buduneli E, Bykoğlu B, Aksu K, Saraç F, Nile C et al. Gingival crevicular fluid, serum levels of receptor activator of nuclear factor-kappaB ligand, osteoprotegerin, and interleukin 17 in patients with rheumatoid arthritis and osteoporosis and with periodontal disease. J Periodontol. 2013; 84 (11): 1627-1637.

  20. Takahashi K, Azuma T, Motohira H, Kinane DF, Kitetsu S. The potential role of interleukin-17 in the immunopathology of periodontal disease. J Clin Periodontol. 2005; 32 (4): 369-374.

  21. Vernal R, Dutzan N, Chaparro A, Puente J, Antonieta VM, Gamonal J. Levels of interleukin-17 in gingival crevicular fluid and in supernatants of cellular cultures of gingival tissue from patients with chronic periodontitis. J Clin Periodontol. 2005; 32 (4): 383-389.

  22. Vernal R, Dutzan N, Hernández M, Chandia S, Puente J, León R et al. High expression levels of receptor activator of nuclear factor-kappa B ligand associated with human chronic periodontitis are mainly secreted by CD4+ T lymphocytes. J Periodontol. 2006; 77 (10): 1772-1780.

  23. Himani GS, Prabhuji ML, Karthikeyan BV. Gingival crevicular fluid and interleukin-23 concentration in systemically healthy subjects: their relationship in periodontal health and disease. J Periodontal Res. 2014; 49 (2): 237-245.

  24. Lester SR, Bain JL, Johnson RB, Serio FG. Gingival concentrations of interleukin-23 and -17 at healthy sites and at sites of clinical attachment loss. Journal of periodontology. 2007; 78 (8): 1545-1550.

  25. Cifcibasi E, Koyuncuoglu C, Ciblak M, Badur S, Kasali K, Firatli E et al. Evaluation of Local and Systemic Levels of Interleukin-17, Interleukin-23, and Myeloperoxidase in Response to Periodontal Therapy in Patients with Generalized Aggressive Periodontitis. Inflammation. 2015; 38 (5): 1959-1968.

  26. Cantín M. Declaración de Helsinki de la Asociación Médica Mundial: Principios éticos para las investigaciones médicas en seres humanos. Revisando su última versión. Int J Med Surg Sci. 2013; 1 (4): 339-346, 2014.

  27. Löe H. The gingival index,the plaque index and the retention index systems. J Periodontol. 1967; 38: 610-616.

  28. Duarte PM, da Rocha M, Sampaio E, Mestnik MJ, Feres M, Figueiredo LC et al. Serum levels of cytokines in subjects with generalized chronic and aggressive periodontitis before and after non-surgical periodontal therapy: a pilot study. J Periodontol. 2010; 81 (7): 1056-1063.

  29. Rosenberg-Hasson Y, Hansmann L, Liedtke M, Herschmann I, Maecker HT. Effects of serum and plasma matrices on multiplex immunoassays. Immunol Res. 2014; 58 (2-3): 224-233.

  30. Lee JE, Kim JW, Han BG, Shin SY. Impact of whole-blood processing conditions on plasma and serum concentrations of cytokines. Biopreserv Biobank. 2016; 14 (1): 51-55.




2020     |     www.medigraphic.com