DIFFERENTIAL EXPRESSION OF INTERLEUKIN-8 AND INTERCELLULAR-ADHESION MOLECULE-1 BY HUMAN GINGIVAL EPITHELIAL-CELLS IN RESPONSE TO ACTINOBACILLUS-ACTINOMYCETEMCOMITANS OR PORPHYROMONAS-GINGIVALIS INFECTION

Citation
Gtj. Huang et al., DIFFERENTIAL EXPRESSION OF INTERLEUKIN-8 AND INTERCELLULAR-ADHESION MOLECULE-1 BY HUMAN GINGIVAL EPITHELIAL-CELLS IN RESPONSE TO ACTINOBACILLUS-ACTINOMYCETEMCOMITANS OR PORPHYROMONAS-GINGIVALIS INFECTION, Oral microbiology and immunology, 13(5), 1998, pp. 301-309
Citations number
47
Categorie Soggetti
Immunology,Microbiology,"Dentistry,Oral Surgery & Medicine
ISSN journal
09020055
Volume
13
Issue
5
Year of publication
1998
Pages
301 - 309
Database
ISI
SICI code
0902-0055(1998)13:5<301:DEOIAI>2.0.ZU;2-Z
Abstract
Little is known regarding the molecules expressed by gingival epitheli al cells that are involved in initiating and maintaining inflammation following the interaction with periodontal pathogens. Thus, we investi gated the effect pf Actinobacillus actinomycetemcomitans and Porphyrom onas gingivalis infection on the expression of neutrophil chemoattract ant interleukin 8 (IL-8) and the adhesion molecule intercellular adhes ion molecule-1 by gingival epithelial cells. The data revealed that bo th IL-8 and intercellular adhesion molecule-1 expression increased aft er infection with A. actinomycetemcomitans (IL-8: 2- to 7-fold; interc ellular adhesion molecule-1: 2.5- to 3.7-fold). IL-8 secretion reached a maximal level 6 h after the infection and the expression subsequent ly decreased to basal level. The increased cell surface intercellular adhesion molecule-1 expression started at 4 h after infection and reac hed a maximal level 14 h after the infection. In contrast, the express ion of both molecules rapidly decreased 2 h after challenge with P. gi ngivalis. This opposite influence of A. actinomycetemcomitans and P. g ingivalis infection on the expression of IL-8 and intercellular adhesi on molecule-1 by gingival epithelial cells suggests that A. actinomyce temcomitans infection may initiate the recruitment of neutrophils, whe reas the P. gingivalis infection may retard this process and therefore demonstrate a distinct perspective of virulence.