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Endotoxin-induced lung inflammation is independent of the complement membrane attack complex
R B Brauer1, C Gegenfurtner, B Neumann
1Department of Surgery, Immunology and Hygiene, Klinikum rechts der Isar, Technische Universität München, D-81675 Munich, Germany. brauer@nt1.chir.med.tu-muenchen.de
Infection and Immunity
|February 26, 2000
Summary
The membrane attack complex (MAC) does not enhance endotoxin-induced lung injury during septic shock. This study found no significant differences in inflammatory responses between rats with and without MAC, suggesting its role in this condition is dispensable.
Area of Science:
- Immunology
- Pathophysiology
Background:
- The membrane attack complex (MAC) (C5b-C9) can enhance tumor necrosis factor alpha (TNF-alpha)-induced expression of selectins and intercellular adhesion molecule type 1 on endothelial cells in vitro.
- Septic shock, often triggered by endotoxins, involves complex inflammatory responses in the lungs.
Purpose of the Study:
- To investigate the in vivo role of the TNF-alpha and MAC synergism in lung injury during endotoxin-mediated septic shock.
- To compare inflammatory responses in C6-deficient rats (lacking MAC) and congenic rats with functional complement.
Main Methods:
- Utilized a rat model of endotoxin-mediated septic shock using lipopolysaccharide (LPS) challenge.
- Compared C6-deficient PVG (C-) rats with congenic PVG (C+) rats.
- Assessed the expression of cytokines, chemokines, and adhesion molecules, along with leukocyte recruitment in the lungs.
Main Results:
- LPS challenge induced significant expression of TNF-alpha, interleukins, chemokines, and P-selectin in both rat strains.
- No significant differences were observed between PVG (C-) and PVG (C+) rats in cytokine/chemokine induction or leukocyte infiltration.
- Lung infiltration by CD11b/c(+) leukocytes was similar in both groups.
Conclusions:
- The in vitro observed synergism between TNF-alpha and MAC in inducing endothelial adhesion molecules is dispensable for inflammatory processes during endotoxin-mediated septic shock in vivo.
- The complement system's MAC is not essential for the development of lung injury in this septic shock model.