•  
  •  
 

Abstract

Cardiovascular and periodontal diseases are common inflammatory conditions in the human population. Tlymphocytes
participate
in
the

pathogenesis and inflammatory events of atherosclerosis. These immune cells enter the
inflamed artery wall and join macrophages via a number of interferon-c-inducible chemokines. Chemokines (IL-8),
cytokines, and growth factors also participate in this process. The interaction between interleukin- 8 and its receptor,
CXCR2, can also contribute to lesion formation in mice. The main causes of aggressive periodontitis is
Actinobacillus
actinomycetemcomitans
. Previous studies have proven that adhesin protein with 24 kDa molecular weight from
A.actinomycetemcomitans is a specific adhesin, this adhesin proteins play a role in the adhesion process on host. this
kind adhesion in the epithelial attachment would lead to colonization and invasion of
A.actinomycetemcomitans that
will stimulate the host immune response. This study aimed to analyze the influence of induction 24 kDa
A.actinomycetemcomitans adhesin protein to the titre of IL-8 in heart of Wistar rat with aggressive periodontitis using
Elisa method to measure and analyze the titre of IL-8. After analyzed with analysis of variance, showed significant
differences of IL-8 titre in the control group and the group with the induction by
A.actinomycetemcomitans,
A.actinomycetemcomitans plus 24 kDa A.actinomycetemcomitans adhesin protein, and only with 24 kDa
A.actinomycetemcomitans adhesin protein. It can be concluded that A.actinomycetemcomitans adhesin protein with 24
kDa molecular weight has a role in increasing of IL-8 titre in heart wistar rat with aggressive periodontitis.

Pages

74-79

Rights

©2016Rini Devijanti Ridwan, Retno Indrawati

DOI

10.15562/jdmfs.v13i2.392

Download

Share

COinS