Gingival concentrations of interleukin-23 and-17 at healthy sites and at sites of clinical attachment loss

被引:91
作者
Lester, S. Reid [1 ]
Bain, Jennifer L. [1 ]
Johnson, Roger B. [1 ]
Serio, Francis G. [1 ]
机构
[1] Univ Mississippi, Med Ctr, Dept Periodont & Prevent Sci, Jackson, MS 39216 USA
关键词
interleukin-12; interleukin-17; interleukin-23; periodontitis;
D O I
10.1902/jop.2007.060458
中图分类号
R78 [口腔科学];
学科分类号
1003 [口腔医学];
摘要
Background: The presence of interleukin (IL)-23 has not been reported within inflamed gingiva, so we evaluated its concentration within gingiva from normal sites and sites of chronic periodontal disease. Methods: Gingiva was obtained prior to extraction of teeth. It was grouped based on clinical attachment loss (CAL): 0 to 2 mm (normal-slight), 3 to 4 mm (moderate), and > 5 mm (severe). Tissues were solubilized, and IL-12, -23, -6, -17, and -1 beta; interferon -gamma (IFN-gamma); and tumor necrosis factor-alpha (TNF-alpha) concentrations were assessed by enzyme-linked immunosorbent assay. Data were compared by factorial analysis of variance, post hoc Tukey test, and Pearson correlation test. Groups were defined as significantly different when P < 0.05. Results: The gingival concentrations of IL-23, -17, -1 beta, and -6 and IFN-gamma were significantly greater at moderate CAL sites than at normal-slight CAL sites. Gingival concentrations of IL-23, -1 beta, -17, and -6 and TNF-alpha. were significantly greater at severe CAL sites than at normal-slight CAL sites. In addition, the gingival concentrations of IL-23, -17, and -6 and TNF-alpha were significantly greater and the gingival concentrations of IL-12 and IFN-gamma were significantly lower at severe CAL sites than at moderate CAL sites. Gingival concentrations of IL-23, -17, -6, and - 1 beta and TNF-alpha correlated positively with CAL. The IL-23 gingival concentration correlated significantly with IL-17, -1 beta, and -6 and TNF-alpha concentrations and correlated negatively with IL-12 and IFN-gamma concentrations. Conclusions: Our results suggested the possibility that the IL-23/IL-17 immune response was present within chronically inflamed gingiva. This is a host response that had not been reported previously in periodontal disease and may be an important factor in the chronic nature of the disease.
引用
收藏
页码:1545 / 1550
页数:6
相关论文
共 46 条
[1]
Aarvak T, 1999, J IMMUNOL, V162, P1246
[2]
Interleukin-23 promotes a distinct CD4 T cell activation state characterized by the production of interleukin-17 [J].
Aggarwal, S ;
Ghilardi, N ;
Xie, MH ;
de Sauvage, FJ ;
Gurney, AL .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2003, 278 (03) :1910-1914
[3]
[Anonymous], 2000, J PERIODONTOL
[4]
Coffman RL, 1999, CURR TOP MICROBIOL, V238, P1
[5]
COFFMAN RL, 1989, HOSP PRACT, V24, P101
[6]
INTERLEUKIN-10 (IL-10) INHIBITS HUMAN LYMPHOCYTE INTERFERON GAMMA-PRODUCTION BY SUPPRESSING NATURAL-KILLER-CELL STIMULATORY FACTOR/IL-12 SYNTHESIS IN ACCESSORY CELLS [J].
DANDREA, A ;
ASTEAMEZAGA, M ;
VALIANTE, NM ;
MA, XJ ;
KUBIN, M ;
TRINCHIERI, G .
JOURNAL OF EXPERIMENTAL MEDICINE, 1993, 178 (03) :1041-1048
[7]
IL-17, produced by lymphocytes and neutrophils, is necessary for lipopolysaccharide-induced airway neutrophilia: IL-15 as a possible trigger [J].
Ferretti, S ;
Bonneau, O ;
Dubois, GR ;
Jones, CE ;
Trifilieff, A .
JOURNAL OF IMMUNOLOGY, 2003, 170 (04) :2106-2112
[8]
T cell interleukin-17 induces stromal cells to produce proinflammatory and hematopoietic cytokines [J].
Fossiez, F ;
Djossou, O ;
Chomarat, P ;
FloresRomo, L ;
AitYahia, S ;
Maat, C ;
Pin, JJ ;
Garrone, P ;
Garcia, E ;
Saeland, S ;
Blanchard, D ;
Gaillard, C ;
DasMahapatra, B ;
Rouvier, E ;
Golstein, P ;
Banchereau, J ;
Lebecque, S .
JOURNAL OF EXPERIMENTAL MEDICINE, 1996, 183 (06) :2593-2603
[9]
GAJEWSKI TF, 1988, J IMMUNOL, V140, P4245
[10]
Immunoregulatory control of Th1/Th2 cytokine profiles in periodontal disease [J].
Gemmell, E ;
Seymour, GJ .
PERIODONTOLOGY 2000, 2004, 35 :21-41