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