Comparison of CCL28, interleukin-8, interleukin-1β and tumor necrosis factor-alpha in subjects with gingivitis, chronic periodontitis and generalized aggressive periodontitis

Background and Objective:  Cytokines produced by various cells are strong local mediators of inflammation. Mucosa‐associated epithelial chemokine (CCL28), interleukin‐8 (IL‐8), interleukin‐1beta (IL‐1β) and tumor necrosis factor‐alpha (TNF‐α) are major cytokines that play important roles in the peri...

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Published inJournal of periodontal research Vol. 48; no. 1; pp. 44 - 51
Main Authors Ertugrul, A. S., Sahin, H., Dikilitas, A., Alpaslan, N., Bozoglan, A.
Format Journal Article
LanguageEnglish
Published Oxford, UK Blackwell Publishing Ltd 01.02.2013
Blackwell
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Abstract Background and Objective:  Cytokines produced by various cells are strong local mediators of inflammation. Mucosa‐associated epithelial chemokine (CCL28), interleukin‐8 (IL‐8), interleukin‐1beta (IL‐1β) and tumor necrosis factor‐alpha (TNF‐α) are major cytokines that play important roles in the periodontal inflammatory process. In this study we aimed to compare the levels of CCL28, IL‐8, IL‐1β and TNF‐α in the gingival crevicular fluid of both periodontally healthy subjects and in subjects diagnosed with gingivitis, chronic periodontitis and generalized aggressive periodontitis. Material and Methods:  A total of 84 subjects participated in the study: 21 subjects had gingivitis, 21 subjects had chronic periodontitis, 21 subjects had generalized aggressive periodontitis and 21 were periodontally healthy. The levels of CCL28, IL‐8, IL‐1β and TNF‐α were analyzed using enzyme‐linked immune sorbent assay (ELISA). Results:  The total levels of CCL28 and IL‐8 in the gingival crevicular fluid of the generalized aggressive periodontitis group (324.74 ± 42.62 pg/30 s, 487.62 ± 49.21 pg/30 s) were significantly higher than those of the chronic periodontitis group (268.81 ± 28.64 pg/30 s, 423.65 ± 35.24 pg/30 s), the gingivitis group (146.35 ± 17.46 pg/30 s, 310.24 ± 48.20 pg/30 s) and the periodontally healthy group (92.46 ± 22.04 pg/30 s, 148.41 ± 24.64 pg/30 s). Similarly, the total levels of IL‐1β and TNF‐α in the generalized aggressive periodontitis group (110.23 ± 9.20 pg/30 s, 1284.46 ± 86.32 pg/30 s) were significantly higher than those in the chronic periodontitis group (423.65 ± 35.24 pg/30 s, 82.64 ± 9.12 pg/30 s), the gingivitis group (52.10 ± 7.15 pg/30 s, 824.24 ± 44.68 pg/30 s) and the periodontally healthy group (36.44 ± 8.86 pg/30 s, 628.26 ± 34.61 pg/30 s). Conclusion:  CCL28, IL‐8, IL‐1β and TNF‐α may play key roles in the host response to inflammation in periodontal diseases. As the severity of periodontal diseases increases, destruction of periodontal tissues also increases. Inflammation is one among many factors that trigger periodontal tissue destruction. Identification of the mediators that influence the development and progression of inflammation in periodontal diseases may be very important in understanding the prognoses of periodontal diseases.
AbstractList Cytokines produced by various cells are strong local mediators of inflammation. Mucosa-associated epithelial chemokine (CCL28), interleukin-8 (IL-8), interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) are major cytokines that play important roles in the periodontal inflammatory process. In this study we aimed to compare the levels of CCL28, IL-8, IL-1β and TNF-α in the gingival crevicular fluid of both periodontally healthy subjects and in subjects diagnosed with gingivitis, chronic periodontitis and generalized aggressive periodontitis. A total of 84 subjects participated in the study: 21 subjects had gingivitis, 21 subjects had chronic periodontitis, 21 subjects had generalized aggressive periodontitis and 21 were periodontally healthy. The levels of CCL28, IL-8, IL-1β and TNF-α were analyzed using enzyme-linked immune sorbent assay (ELISA). The total levels of CCL28 and IL-8 in the gingival crevicular fluid of the generalized aggressive periodontitis group (324.74 ± 42.62 pg/30 s, 487.62 ± 49.21 pg/30 s) were significantly higher than those of the chronic periodontitis group (268.81 ± 28.64 pg/30 s, 423.65 ± 35.24 pg/30 s), the gingivitis group (146.35 ± 17.46 pg/30 s, 310.24 ± 48.20 pg/30 s) and the periodontally healthy group (92.46 ± 22.04 pg/30 s, 148.41 ± 24.64 pg/30 s). Similarly, the total levels of IL-1β and TNF-α in the generalized aggressive periodontitis group (110.23 ± 9.20 pg/30 s, 1284.46 ± 86.32 pg/30 s) were significantly higher than those in the chronic periodontitis group (423.65 ± 35.24 pg/30 s, 82.64 ± 9.12 pg/30 s), the gingivitis group (52.10 ± 7.15 pg/30 s, 824.24 ± 44.68 pg/30 s) and the periodontally healthy group (36.44 ± 8.86 pg/30 s, 628.26 ± 34.61 pg/30 s). CCL28, IL-8, IL-1β and TNF-α may play key roles in the host response to inflammation in periodontal diseases. As the severity of periodontal diseases increases, destruction of periodontal tissues also increases. Inflammation is one among many factors that trigger periodontal tissue destruction. Identification of the mediators that influence the development and progression of inflammation in periodontal diseases may be very important in understanding the prognoses of periodontal diseases.
Background and Objective:  Cytokines produced by various cells are strong local mediators of inflammation. Mucosa‐associated epithelial chemokine (CCL28), interleukin‐8 (IL‐8), interleukin‐1beta (IL‐1β) and tumor necrosis factor‐alpha (TNF‐α) are major cytokines that play important roles in the periodontal inflammatory process. In this study we aimed to compare the levels of CCL28, IL‐8, IL‐1β and TNF‐α in the gingival crevicular fluid of both periodontally healthy subjects and in subjects diagnosed with gingivitis, chronic periodontitis and generalized aggressive periodontitis. Material and Methods:  A total of 84 subjects participated in the study: 21 subjects had gingivitis, 21 subjects had chronic periodontitis, 21 subjects had generalized aggressive periodontitis and 21 were periodontally healthy. The levels of CCL28, IL‐8, IL‐1β and TNF‐α were analyzed using enzyme‐linked immune sorbent assay (ELISA). Results:  The total levels of CCL28 and IL‐8 in the gingival crevicular fluid of the generalized aggressive periodontitis group (324.74 ± 42.62 pg/30 s, 487.62 ± 49.21 pg/30 s) were significantly higher than those of the chronic periodontitis group (268.81 ± 28.64 pg/30 s, 423.65 ± 35.24 pg/30 s), the gingivitis group (146.35 ± 17.46 pg/30 s, 310.24 ± 48.20 pg/30 s) and the periodontally healthy group (92.46 ± 22.04 pg/30 s, 148.41 ± 24.64 pg/30 s). Similarly, the total levels of IL‐1β and TNF‐α in the generalized aggressive periodontitis group (110.23 ± 9.20 pg/30 s, 1284.46 ± 86.32 pg/30 s) were significantly higher than those in the chronic periodontitis group (423.65 ± 35.24 pg/30 s, 82.64 ± 9.12 pg/30 s), the gingivitis group (52.10 ± 7.15 pg/30 s, 824.24 ± 44.68 pg/30 s) and the periodontally healthy group (36.44 ± 8.86 pg/30 s, 628.26 ± 34.61 pg/30 s). Conclusion:  CCL28, IL‐8, IL‐1β and TNF‐α may play key roles in the host response to inflammation in periodontal diseases. As the severity of periodontal diseases increases, destruction of periodontal tissues also increases. Inflammation is one among many factors that trigger periodontal tissue destruction. Identification of the mediators that influence the development and progression of inflammation in periodontal diseases may be very important in understanding the prognoses of periodontal diseases.
Cytokines produced by various cells are strong local mediators of inflammation. Mucosa-associated epithelial chemokine (CCL28), interleukin-8 (IL-8), interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) are major cytokines that play important roles in the periodontal inflammatory process. In this study we aimed to compare the levels of CCL28, IL-8, IL-1β and TNF-α in the gingival crevicular fluid of both periodontally healthy subjects and in subjects diagnosed with gingivitis, chronic periodontitis and generalized aggressive periodontitis.BACKGROUND AND OBJECTIVECytokines produced by various cells are strong local mediators of inflammation. Mucosa-associated epithelial chemokine (CCL28), interleukin-8 (IL-8), interleukin-1beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) are major cytokines that play important roles in the periodontal inflammatory process. In this study we aimed to compare the levels of CCL28, IL-8, IL-1β and TNF-α in the gingival crevicular fluid of both periodontally healthy subjects and in subjects diagnosed with gingivitis, chronic periodontitis and generalized aggressive periodontitis.A total of 84 subjects participated in the study: 21 subjects had gingivitis, 21 subjects had chronic periodontitis, 21 subjects had generalized aggressive periodontitis and 21 were periodontally healthy. The levels of CCL28, IL-8, IL-1β and TNF-α were analyzed using enzyme-linked immune sorbent assay (ELISA).MATERIAL AND METHODSA total of 84 subjects participated in the study: 21 subjects had gingivitis, 21 subjects had chronic periodontitis, 21 subjects had generalized aggressive periodontitis and 21 were periodontally healthy. The levels of CCL28, IL-8, IL-1β and TNF-α were analyzed using enzyme-linked immune sorbent assay (ELISA).The total levels of CCL28 and IL-8 in the gingival crevicular fluid of the generalized aggressive periodontitis group (324.74 ± 42.62 pg/30 s, 487.62 ± 49.21 pg/30 s) were significantly higher than those of the chronic periodontitis group (268.81 ± 28.64 pg/30 s, 423.65 ± 35.24 pg/30 s), the gingivitis group (146.35 ± 17.46 pg/30 s, 310.24 ± 48.20 pg/30 s) and the periodontally healthy group (92.46 ± 22.04 pg/30 s, 148.41 ± 24.64 pg/30 s). Similarly, the total levels of IL-1β and TNF-α in the generalized aggressive periodontitis group (110.23 ± 9.20 pg/30 s, 1284.46 ± 86.32 pg/30 s) were significantly higher than those in the chronic periodontitis group (423.65 ± 35.24 pg/30 s, 82.64 ± 9.12 pg/30 s), the gingivitis group (52.10 ± 7.15 pg/30 s, 824.24 ± 44.68 pg/30 s) and the periodontally healthy group (36.44 ± 8.86 pg/30 s, 628.26 ± 34.61 pg/30 s).RESULTSThe total levels of CCL28 and IL-8 in the gingival crevicular fluid of the generalized aggressive periodontitis group (324.74 ± 42.62 pg/30 s, 487.62 ± 49.21 pg/30 s) were significantly higher than those of the chronic periodontitis group (268.81 ± 28.64 pg/30 s, 423.65 ± 35.24 pg/30 s), the gingivitis group (146.35 ± 17.46 pg/30 s, 310.24 ± 48.20 pg/30 s) and the periodontally healthy group (92.46 ± 22.04 pg/30 s, 148.41 ± 24.64 pg/30 s). Similarly, the total levels of IL-1β and TNF-α in the generalized aggressive periodontitis group (110.23 ± 9.20 pg/30 s, 1284.46 ± 86.32 pg/30 s) were significantly higher than those in the chronic periodontitis group (423.65 ± 35.24 pg/30 s, 82.64 ± 9.12 pg/30 s), the gingivitis group (52.10 ± 7.15 pg/30 s, 824.24 ± 44.68 pg/30 s) and the periodontally healthy group (36.44 ± 8.86 pg/30 s, 628.26 ± 34.61 pg/30 s).CCL28, IL-8, IL-1β and TNF-α may play key roles in the host response to inflammation in periodontal diseases. As the severity of periodontal diseases increases, destruction of periodontal tissues also increases. Inflammation is one among many factors that trigger periodontal tissue destruction. Identification of the mediators that influence the development and progression of inflammation in periodontal diseases may be very important in understanding the prognoses of periodontal diseases.CONCLUSIONCCL28, IL-8, IL-1β and TNF-α may play key roles in the host response to inflammation in periodontal diseases. As the severity of periodontal diseases increases, destruction of periodontal tissues also increases. Inflammation is one among many factors that trigger periodontal tissue destruction. Identification of the mediators that influence the development and progression of inflammation in periodontal diseases may be very important in understanding the prognoses of periodontal diseases.
Background and Objective:  Cytokines produced by various cells are strong local mediators of inflammation. Mucosa‐associated epithelial chemokine (CCL28), interleukin‐8 (IL‐8), interleukin‐1beta (IL‐1β) and tumor necrosis factor‐alpha (TNF‐α) are major cytokines that play important roles in the periodontal inflammatory process. In this study we aimed to compare the levels of CCL28, IL‐8, IL‐1β and TNF‐α in the gingival crevicular fluid of both periodontally healthy subjects and in subjects diagnosed with gingivitis, chronic periodontitis and generalized aggressive periodontitis. Material and Methods:  A total of 84 subjects participated in the study: 21 subjects had gingivitis, 21 subjects had chronic periodontitis, 21 subjects had generalized aggressive periodontitis and 21 were periodontally healthy. The levels of CCL28, IL‐8, IL‐1β and TNF‐α were analyzed using enzyme‐linked immune sorbent assay (ELISA). Results:  The total levels of CCL28 and IL‐8 in the gingival crevicular fluid of the generalized aggressive periodontitis group (324.74 ± 42.62 pg/30 s, 487.62 ± 49.21 pg/30 s) were significantly higher than those of the chronic periodontitis group (268.81 ± 28.64 pg/30 s, 423.65 ± 35.24 pg/30 s), the gingivitis group (146.35 ± 17.46 pg/30 s, 310.24 ± 48.20 pg/30 s) and the periodontally healthy group (92.46 ± 22.04 pg/30 s, 148.41 ± 24.64 pg/30 s). Similarly, the total levels of IL‐1β and TNF‐α in the generalized aggressive periodontitis group (110.23 ± 9.20 pg/30 s, 1284.46 ± 86.32 pg/30 s) were significantly higher than those in the chronic periodontitis group (423.65 ± 35.24 pg/30 s, 82.64 ± 9.12 pg/30 s), the gingivitis group (52.10 ± 7.15 pg/30 s, 824.24 ± 44.68 pg/30 s) and the periodontally healthy group (36.44 ± 8.86 pg/30 s, 628.26 ± 34.61 pg/30 s). Conclusion:  CCL28, IL‐8, IL‐1β and TNF‐α may play key roles in the host response to inflammation in periodontal diseases. As the severity of periodontal diseases increases, destruction of periodontal tissues also increases. Inflammation is one among many factors that trigger periodontal tissue destruction. Identification of the mediators that influence the development and progression of inflammation in periodontal diseases may be very important in understanding the prognoses of periodontal diseases.
Author Sahin, H.
Alpaslan, N.
Ertugrul, A. S.
Bozoglan, A.
Dikilitas, A.
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  organization: Department of Periodontology, Faculty of Dentistry, Yuzuncu Yil University, Van, Turkey
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https://www.ncbi.nlm.nih.gov/pubmed/22812409$$D View this record in MEDLINE/PubMed
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ISSN 0022-3484
1600-0765
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IsPeerReviewed true
IsScholarly true
Issue 1
Keywords Human
Stomatology
chronic periodontitis
Cytokine
Interleukin 1β
chemokines
Gingivitis
Generalized
Chemokine
Periodontal disease
Chronic
Periodontitis
aggressive periodontitis
cytokines
gingival crevice fluid
Comparative study
Tumor necrosis factor α
Interleukin 8
Gingival fluid
Language English
License http://onlinelibrary.wiley.com/termsAndConditions#vor
CC BY 4.0
2012 John Wiley & Sons A/S.
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PublicationDate February 2013
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  year: 2013
  text: February 2013
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PublicationPlace Oxford, UK
PublicationPlace_xml – name: Oxford, UK
– name: Oxford
– name: United States
PublicationTitle Journal of periodontal research
PublicationTitleAlternate J Periodontal Res
PublicationYear 2013
Publisher Blackwell Publishing Ltd
Blackwell
Publisher_xml – name: Blackwell Publishing Ltd
– name: Blackwell
References Kagami S, Kakinuma T, Saeki H et al. Increased serum CCL28 levels in patients with atopic dermatitis, psoriasis vulgaris and bullous pemphigoid. J Invest Dermatol2005;124:1088-1090.
Sorsa T, Tervahartiala T, Leppilahti J et al. Collagenase-2 (MMP-8) as a point-of-care biomarker in periodontitis and cardiovascular diseases. therapeutic response to non-antimicrobial properties of tetracyclines. Pharmacol Res2011;63:108-113.
Birkedal-Hansen H. Role of cytokines and inflammatory mediators in tissue destruction. J Periodontal Res1993;28:500-510.
Wilson ME, Zambon JJ, Suzuki JB, Genco RJ. Generalized juvenile periodontitis, defective neutrophil chemotaxis and bacteriodes gingivalis in a 13-year-old female. A case report. J Periodontol1985;56:457-462.
Silness P, Löe H. Periodontal disease in pregnancy. Acta Odontol Scand1964;22:121.
Eksteen B, Miles A, Curbishley SM et al. Epithelial inflammation is associated with CCL28 production and the recruitment of regulatory T cells expressing CCR10. J Immunol2006;177:593-603.
Öztürk A, Yildız L. Expression of transient receptor potential vanilloid receptor 1 and toll-like receptor 4 in aggressive periodontitis and in chronic periodontitis. J Periodontal Res2011;46:475-482.
Liu B, Wilson E. The antimicrobial activity of CCL28 is dependent on C-terminal positively-charged amino acids. Eur J Immunol2010;40:186-196.
Elsner J, Mack M, Brühl H et al. Differential activation of CC chemokine receptors by AOP-RANTES. J Biol Chem2000;275:7787-7794.
Glavind L, Löe H. Errors in the clinical assessment of periodontal destruction. J Periodontal Res1967;2:180-184.
Löe H. The gingival index, the plaque index and the retantion index systems. J Clin Periodontol1967;38:61-70.
Hieshima K, Ohtani H, Shibano M et al. CCL28 has dual roles in mucosal immunity as a chemokine with broad-spectrum antimicrobial activity. J Immunol2003;170:1452-1461.
Kinane DF, Lappin DF. Clinical, pathological and immunological aspects of periodontal disease. Acta Odontol Scand2001;59:154-160.
Lamster IB, Novak MJ. Host mediators in gingival crevicular fluid: implications for the pathogenesis of periodontal disease. Crit Rev Oral Biol Med1992;3:31-60.
John AE, Thomas MS, Berlin AA, Lukacs NW. Temporal production of CCL28 corresponds to eosinophil accumulation and airway hyperreactivity in allergic airway inflammation. Int J Immunogenet2005;166:345-353.
Preshaw PM. Host response modulation in periodontics. Periodontol 20002008;48:92-110.
Zhong Y, Slade GD, Beck JD, Offenbacher S. Gingival crevicular fluid interleukin-1beta, prostaglandin E2 and periodontal status in a community population. J Periodontol2007;34:285-293.
Kinane DF, Podmore M, Ebersole J. Etiopathogenesis of periodontitis in children and adolescents. Periodontol 20002001;26:54-91.
Ogawa H, Iimura M, Eckmann L, Kagnoff MF. Regulated production of the chemokine CCL28 in human colon epithelium. Am J Physiol Gastrointest Liver Physiol2004;287:G1062-G1069.
Goebeler M, Trautmann A, Voss A, Brocker EV, Toksoy A, Gillitzer R. Differential and sequential expression of multiple chemokines during elicitation of allergic contact hypersensitivity. Am J Pathol2001;158:431-440.
Gamonal J, Acevedo A, Bascones A, Jorge O, Silva A. Levels of interleukin-1β, -8 and -10 and RANTES in gingival crevicular fluid and cell populations in adult periodontitis patients and the effect of periodontal treatment. J Periodontol2000;71:1535-1545.
Orozco A, Gemmell E, Bickel M, Seymour GJ. Interleukin-1beta, interleukin-12 and interleukin-18 levels in gingival fluid and serum of patients with gingivitis and periodontitis. Oral Microbiol Immunol2006;21:256-260.
Sorsa T, Mäntylä P, Tervahartiala T, Pussinen PJ, Gamonal J, Hernandez M. MMP activation in diagnostics of periodontitis and systemic inflammation. J Clin Periodontol2011;38:817-819.
Graves DT, Cochran D. The contribution of interleukin-1 and tumor necrosis factor to periodontal tissue destruction. J Periodontol2003;74:391-401.
Meikle MC, Atkinson SJ, Ward RV, Murphy G, Reynolds JJ. Gingival fibroblasts degrade type I collagen films when stimulated with tumor necrosis factor and interleukin 1: evidence that breakdown is mediated by metalloproteinases. J Periodontal Res1989;24:207-213.
Loetscher P, Moser B, Baggiolini M. Chemokines and their receptors in lymphocyte traffic and HIV infection. Adv Immunol2000;74:127-128.
Okada H, Murakami S. Cytokine expression in periodontal health and disease. Crit Rev Oral Biol Med1998;9:248-266.
Feng N, Jaimes MC, Lazarus NH et al. Redundant role of chemokines CCL25/TECK and CCL28/MEC in IgA+ plasmablast recruitment to the intestinal lamina propria after rotavirus infection. J Immunol2006;176:5749-5759.
Van Dyke TE, Serhan CN. Resolution of inflammation: a new paradigm for the pathogenesis of periodontal diseases. J Periodontal Res2003;82:82-90.
Tsai C, Ho Y, Chen C. Levels of interleukin-1β and interleukin-8 in gingival crevicular fluids in adult periodontitis. J Periodontol1995;66:852-859.
Pradeep AR, Raghavendra NM, Prasad MV, Kathariya R, Patel SP, Sharma A. Gingival crevicular fluid and serum visfatin concentration: their relationship in periodontal health and disease. J Periodontol2011;82:1314-1319.
Chen RH, Chen WC, Wang TY, Tsai CH. Lack of association between pro-inflammatory cytokine (IL6-8, TNF-alpha) gene polymorphism and graves disease. Int J Immunogenet2005;32:343-347.
Ying S, Meng Q, Zeibecoglou K et al. Eosinophil chemotactic chemokines (eotaxin, eotaxin-2, RANTES, monocyte chemoattractant protein-3 (MCP-3), and MCP-4), and C-C chemokine receptor 3 expression in bronchial biopsies from atopic and nonatopic (Intrinsic) asthmatics. J Immunol1999;163:6321-6329.
English K, Brady C, Corcoran P, Cassidy JP, Mahon BP. Inflammation of the respiratory tract is associated with CCL28 and CCR10 expression in a murine model of allergic asthma. Immunol Lett2006;103:92-100.
Ezzat MH, Sallam MA, Shaheen KY. Serum mucosa-associated epithelial chemokine (MEC/CCL28) in atopic dermatitis: a specific marker for severity. Int J Dermatol2009;48:822-829.
Senturk T, Kozaci LD, Kok F, Kadikoylu G, Bolaman Z. Proinflammatory cytokine levels in hyperthyroidism. Clin Invest Med2003;26:58-63.
Griffiths GS, Ayob R, Guerrero A et al. Amoxicillin and metronidazole as an adjunctive treatment in generalized aggressive periodontitis at initial therapy or re-treatment: a randomized controlled clinical trial. J Clin Periodontol2011;38:43-49.
Wang W, Soto H, Oldham ER et al. Identification of a novel chemokine (CCL28), which binds CCR10 (GPR2). J Biol Chem2000;275:22313-22323.
Horuk R, Ng HP. Chemokine receptor antagonists. Med Res Rev2000;20:155-168.
Oliveira AP, Faveri MD, Gursky LC et al. Effects of periodontal therapy on GCF cytokines in generalized aggressive periodontitis subjects. J Clin Periodontol2012;39:295-302.
Mäntylä P, Stenman M, Kinane DF et al. Gingival crevicular fluid collagenase-2 (MMP-8) test stick for chair-side monitoring of periodontitis. J Periodontal Res2003;38:436-439.
Megson E, Fitzsimmons T, Dharmapatni K, Bartold P. C-reactive protein in gingival crevicular fluid may be indicative of systemic inflammation. J Clin Periodontol2010;37:797-804.
Xie YF, Shu R, Jiang SY, Liu DL, Zhang XL. Comparison of microRNA profiles of human periodontal diseased and healthy gingival tissues. Int J Oral Sci2011;3:125-134.
Hansson M, Hermansson M, Svensson H et al. CCL28 is increased in human Helicobacter pylori-induced gastritis and mediates recruitment of gastric immunoglobulin A-secreting cells. Infect Immun2008;76:3304-3311.
Politz O, Kodelja V, Guillot P, Orfanos CE, Goerdt S. Pseudoexons and regulatory elements in the genomic sequence of the beta-chemokine, alternative macrophage activation-associated CC-chemokine (AMAC)-1. Cytokine2000;12:120-126.
Kim CH, Rott L, Kunkel EJ et al. Rules of chemokine receptor association with T cell polarization in vivo. J Clin Invest2001;108:1331-1339.
Teran LM. CCL chemokines and asthma. Immunol Today2000;21:235-241.
Kunkel EJ, Boisvert J, Murphy K et al. Expression of the chemokine receptors CCR4, CCR5, and CXCR3 by human tissue-infiltrating lymphocytes. Am J Pathol2002;160:347-355.
Mathur A, Yang C, Wolff L. Cytokines in gingival crevicular fluid of periodontally disseased and healthy sites. J Periodontal Res1996;31:489-495.
Chung RM, Grbic JT, Lamster IB. Interleukin-8 and β-glucuronidase in gingival crevicular fluid. J Clin Periodontol1997;24:146-152.
Luster AD. Chemokines-chemotactic cytokines that mediate inflammation. N Engl J Med1998;338:436-445.
Preiss DS, Meyle J. Interleukin-1 beta concentration of gingival crevicular fluid. J Periodontol1994;65:423-428.
Watkins HR, Lapp CA, Hanes PJ et al. CCL28 effects on periodontal pathogens. J Periodontol2007;78:2356-2363.
Armitage GC. Development of a classification system for periodontal diseases and conditions. Ann Periodontol1999;4:1-6.
Allen SJ, Crown SE, Handel TM. Chemokine: receptor structure, interactions, and antagonism. Annu Rev Immunol2007;25:787-820.
Özmeriç N, Bal B, Baloş K, Berker E, Bulut S. The correlation of gingival crevicular fluid interleukin-8 levels and periodontal status in localized juvenile periodontitis. J Periodontol1998;69:1299-1304.
2004; 287
1993; 28
2006; 176
1999; 163
2008; 76
2001; 108
2007; 78
2007; 34
2009; 48
2006; 177
1996; 31
1994; 65
2000; 12
2006; 21
1995; 66
2011; 63
2005; 32
2001; 59
2003; 82
1985; 56
1992; 3
2007; 25
2010; 37
2000; 21
2011; 82
1997; 24
2000; 20
1964; 22
1998; 338
2003; 170
2003; 38
2000; 71
2001; 26
1999; 4
2000; 275
2012; 39
2002
2011; 3
2011; 38
1989; 24
2003; 74
2010; 40
1998; 69
2002; 160
2005; 166
2005; 124
1967; 2
2000; 74
2008; 48
2003; 26
2011; 46
1967; 38
2001; 158
1998; 9
2006; 103
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References_xml – reference: Pradeep AR, Raghavendra NM, Prasad MV, Kathariya R, Patel SP, Sharma A. Gingival crevicular fluid and serum visfatin concentration: their relationship in periodontal health and disease. J Periodontol2011;82:1314-1319.
– reference: Hieshima K, Ohtani H, Shibano M et al. CCL28 has dual roles in mucosal immunity as a chemokine with broad-spectrum antimicrobial activity. J Immunol2003;170:1452-1461.
– reference: Xie YF, Shu R, Jiang SY, Liu DL, Zhang XL. Comparison of microRNA profiles of human periodontal diseased and healthy gingival tissues. Int J Oral Sci2011;3:125-134.
– reference: Ying S, Meng Q, Zeibecoglou K et al. Eosinophil chemotactic chemokines (eotaxin, eotaxin-2, RANTES, monocyte chemoattractant protein-3 (MCP-3), and MCP-4), and C-C chemokine receptor 3 expression in bronchial biopsies from atopic and nonatopic (Intrinsic) asthmatics. J Immunol1999;163:6321-6329.
– reference: Wang W, Soto H, Oldham ER et al. Identification of a novel chemokine (CCL28), which binds CCR10 (GPR2). J Biol Chem2000;275:22313-22323.
– reference: Graves DT, Cochran D. The contribution of interleukin-1 and tumor necrosis factor to periodontal tissue destruction. J Periodontol2003;74:391-401.
– reference: Löe H. The gingival index, the plaque index and the retantion index systems. J Clin Periodontol1967;38:61-70.
– reference: Öztürk A, Yildız L. Expression of transient receptor potential vanilloid receptor 1 and toll-like receptor 4 in aggressive periodontitis and in chronic periodontitis. J Periodontal Res2011;46:475-482.
– reference: Ogawa H, Iimura M, Eckmann L, Kagnoff MF. Regulated production of the chemokine CCL28 in human colon epithelium. Am J Physiol Gastrointest Liver Physiol2004;287:G1062-G1069.
– reference: Eksteen B, Miles A, Curbishley SM et al. Epithelial inflammation is associated with CCL28 production and the recruitment of regulatory T cells expressing CCR10. J Immunol2006;177:593-603.
– reference: Watkins HR, Lapp CA, Hanes PJ et al. CCL28 effects on periodontal pathogens. J Periodontol2007;78:2356-2363.
– reference: Kunkel EJ, Boisvert J, Murphy K et al. Expression of the chemokine receptors CCR4, CCR5, and CXCR3 by human tissue-infiltrating lymphocytes. Am J Pathol2002;160:347-355.
– reference: Glavind L, Löe H. Errors in the clinical assessment of periodontal destruction. J Periodontal Res1967;2:180-184.
– reference: Wilson ME, Zambon JJ, Suzuki JB, Genco RJ. Generalized juvenile periodontitis, defective neutrophil chemotaxis and bacteriodes gingivalis in a 13-year-old female. A case report. J Periodontol1985;56:457-462.
– reference: Chen RH, Chen WC, Wang TY, Tsai CH. Lack of association between pro-inflammatory cytokine (IL6-8, TNF-alpha) gene polymorphism and graves disease. Int J Immunogenet2005;32:343-347.
– reference: Mathur A, Yang C, Wolff L. Cytokines in gingival crevicular fluid of periodontally disseased and healthy sites. J Periodontal Res1996;31:489-495.
– reference: Griffiths GS, Ayob R, Guerrero A et al. Amoxicillin and metronidazole as an adjunctive treatment in generalized aggressive periodontitis at initial therapy or re-treatment: a randomized controlled clinical trial. J Clin Periodontol2011;38:43-49.
– reference: Politz O, Kodelja V, Guillot P, Orfanos CE, Goerdt S. Pseudoexons and regulatory elements in the genomic sequence of the beta-chemokine, alternative macrophage activation-associated CC-chemokine (AMAC)-1. Cytokine2000;12:120-126.
– reference: Liu B, Wilson E. The antimicrobial activity of CCL28 is dependent on C-terminal positively-charged amino acids. Eur J Immunol2010;40:186-196.
– reference: Loetscher P, Moser B, Baggiolini M. Chemokines and their receptors in lymphocyte traffic and HIV infection. Adv Immunol2000;74:127-128.
– reference: Kagami S, Kakinuma T, Saeki H et al. Increased serum CCL28 levels in patients with atopic dermatitis, psoriasis vulgaris and bullous pemphigoid. J Invest Dermatol2005;124:1088-1090.
– reference: Zhong Y, Slade GD, Beck JD, Offenbacher S. Gingival crevicular fluid interleukin-1beta, prostaglandin E2 and periodontal status in a community population. J Periodontol2007;34:285-293.
– reference: Van Dyke TE, Serhan CN. Resolution of inflammation: a new paradigm for the pathogenesis of periodontal diseases. J Periodontal Res2003;82:82-90.
– reference: Goebeler M, Trautmann A, Voss A, Brocker EV, Toksoy A, Gillitzer R. Differential and sequential expression of multiple chemokines during elicitation of allergic contact hypersensitivity. Am J Pathol2001;158:431-440.
– reference: Preshaw PM. Host response modulation in periodontics. Periodontol 20002008;48:92-110.
– reference: Meikle MC, Atkinson SJ, Ward RV, Murphy G, Reynolds JJ. Gingival fibroblasts degrade type I collagen films when stimulated with tumor necrosis factor and interleukin 1: evidence that breakdown is mediated by metalloproteinases. J Periodontal Res1989;24:207-213.
– reference: Feng N, Jaimes MC, Lazarus NH et al. Redundant role of chemokines CCL25/TECK and CCL28/MEC in IgA+ plasmablast recruitment to the intestinal lamina propria after rotavirus infection. J Immunol2006;176:5749-5759.
– reference: Silness P, Löe H. Periodontal disease in pregnancy. Acta Odontol Scand1964;22:121.
– reference: Horuk R, Ng HP. Chemokine receptor antagonists. Med Res Rev2000;20:155-168.
– reference: Preiss DS, Meyle J. Interleukin-1 beta concentration of gingival crevicular fluid. J Periodontol1994;65:423-428.
– reference: Elsner J, Mack M, Brühl H et al. Differential activation of CC chemokine receptors by AOP-RANTES. J Biol Chem2000;275:7787-7794.
– reference: Kinane DF, Lappin DF. Clinical, pathological and immunological aspects of periodontal disease. Acta Odontol Scand2001;59:154-160.
– reference: Sorsa T, Mäntylä P, Tervahartiala T, Pussinen PJ, Gamonal J, Hernandez M. MMP activation in diagnostics of periodontitis and systemic inflammation. J Clin Periodontol2011;38:817-819.
– reference: Tsai C, Ho Y, Chen C. Levels of interleukin-1β and interleukin-8 in gingival crevicular fluids in adult periodontitis. J Periodontol1995;66:852-859.
– reference: Okada H, Murakami S. Cytokine expression in periodontal health and disease. Crit Rev Oral Biol Med1998;9:248-266.
– reference: Ezzat MH, Sallam MA, Shaheen KY. Serum mucosa-associated epithelial chemokine (MEC/CCL28) in atopic dermatitis: a specific marker for severity. Int J Dermatol2009;48:822-829.
– reference: Özmeriç N, Bal B, Baloş K, Berker E, Bulut S. The correlation of gingival crevicular fluid interleukin-8 levels and periodontal status in localized juvenile periodontitis. J Periodontol1998;69:1299-1304.
– reference: Gamonal J, Acevedo A, Bascones A, Jorge O, Silva A. Levels of interleukin-1β, -8 and -10 and RANTES in gingival crevicular fluid and cell populations in adult periodontitis patients and the effect of periodontal treatment. J Periodontol2000;71:1535-1545.
– reference: Oliveira AP, Faveri MD, Gursky LC et al. Effects of periodontal therapy on GCF cytokines in generalized aggressive periodontitis subjects. J Clin Periodontol2012;39:295-302.
– reference: Senturk T, Kozaci LD, Kok F, Kadikoylu G, Bolaman Z. Proinflammatory cytokine levels in hyperthyroidism. Clin Invest Med2003;26:58-63.
– reference: Mäntylä P, Stenman M, Kinane DF et al. Gingival crevicular fluid collagenase-2 (MMP-8) test stick for chair-side monitoring of periodontitis. J Periodontal Res2003;38:436-439.
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Snippet Background and Objective:  Cytokines produced by various cells are strong local mediators of inflammation. Mucosa‐associated epithelial chemokine (CCL28),...
Background and Objective:  Cytokines produced by various cells are strong local mediators of inflammation. Mucosa‐associated epithelial chemokine (CCL28),...
Cytokines produced by various cells are strong local mediators of inflammation. Mucosa-associated epithelial chemokine (CCL28), interleukin-8 (IL-8),...
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SubjectTerms Adolescent
Adult
aggressive periodontitis
Aggressive Periodontitis - immunology
Alveolar Bone Loss - immunology
Biological and medical sciences
chemokines
Chemokines, CC - analysis
chronic periodontitis
Chronic Periodontitis - immunology
cytokines
Facial bones, jaws, teeth, parodontium: diseases, semeiology
Female
gingival crevice fluid
Gingival Crevicular Fluid - immunology
Gingival Hemorrhage - immunology
Gingivitis - immunology
Humans
Immunity, Mucosal - immunology
Interleukin-1beta - analysis
Interleukin-8 - analysis
Male
Medical sciences
Non tumoral diseases
Otorhinolaryngology. Stomatology
Periodontal Attachment Loss - immunology
Periodontal Pocket - immunology
Periodontium - immunology
Tumor Necrosis Factor-alpha - analysis
Young Adult
Title Comparison of CCL28, interleukin-8, interleukin-1β and tumor necrosis factor-alpha in subjects with gingivitis, chronic periodontitis and generalized aggressive periodontitis
URI https://api.istex.fr/ark:/67375/WNG-K1G881BR-H/fulltext.pdf
https://onlinelibrary.wiley.com/doi/abs/10.1111%2Fj.1600-0765.2012.01500.x
https://www.ncbi.nlm.nih.gov/pubmed/22812409
https://www.proquest.com/docview/1273126019
Volume 48
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