Endotoxin challenge causes a proinflammatory state in obstructive jaundice


Yorganci K., Baykal A., Kologlu M., Saribas Z., Hascelik G., Sayek I.

JOURNAL OF INVESTIGATIVE SURGERY, vol.17, no.3, pp.119-126, 2004 (SCI-Expanded) identifier

  • Publication Type: Article / Article
  • Volume: 17 Issue: 3
  • Publication Date: 2004
  • Doi Number: 10.1080/08941930490446892
  • Journal Name: JOURNAL OF INVESTIGATIVE SURGERY
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.119-126
  • Hacettepe University Affiliated: Yes

Abstract

The aim of this study was to investigate the relationship between the obstructive jaundice-induced cellular immune suppression and endotoxin challenge with respect to the levels of tumor necrosis factor (TNF), interleukin-10 (IL-10), and interleukin-2 (IL-2). Rats underwent either bile duct ligation or sham operation. At 21 days, all rats were challenged either with lipopolysaccharide (LPS) or saline. In the sham-operated group LPS injection significantly increased TNF levels at 90 min. The common bile duct ligated group showed a significant increase in TNF levels compared with all other groups, including the sham-operated, LPS-injected group, at 90 min. At 180 min following LPS challenge, TNF levels decreased, and there was no difference between any of the LPS-challenged groups at 180 min and any of the saline groups at either 90 or 180 min. In the sham-operated group, LPS injection significantly increased IL-10 levels at both 90 and 180 min. In the bile duct ligated group, LPS injection significantly increased IL-10 levels compared with saline injection at both 90 and 180 min. On the other hand, bile duct ligated animals had significantly less increase in IL-10 levels following LPS challenge at 90 min but not at 180 min. In common bile duct ligated rats, LPS challenge induced a significantly greater increase in IL-2 levels compared with all other groups. In conclusion, in the presence of obstructive jaundice, endotoxemia primes a more vigorous inflammatory response despite cellular immune depression.