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Splenectomy alters Kupffer cell response to endotoxin
T R Billiar1, M A West, B J Hyland
1Veterans of Foreign Wars Cancer Research Center, University of Minnesota Health Sciences Center, Minneapolis.
Archives of Surgery (Chicago, Ill. : 1960)
|March 1, 1988
Summary
Splenectomy reduces Kupffer cell responsiveness to lipopolysaccharide (LPS) by removing splenic lymphokines. This decreased sensitivity may increase infection risk after spleen removal.
Area of Science:
- Immunology
- Cell Biology
- Pathophysiology
Background:
- The spleen produces lymphokines that activate macrophages.
- Kupffer cells in the liver are exposed to splenic factors via portal circulation.
- Splenectomy may alter Kupffer cell function and response to pathogens.
Purpose of the Study:
- To investigate the impact of splenectomy on Kupffer cell responses to lipopolysaccharide (LPS).
- To determine if splenic factors influence Kupffer cell activation by LPS.
Main Methods:
- Utilized an in vitro rat hepatocyte-Kupffer cell coculture system.
- Assessed Kupffer cell activation by measuring its effect on hepatocyte protein synthesis.
- Compared Kupffer cell responses in splenectomized rats versus sham-operated controls.
Main Results:
- Kupffer cells from splenectomized rats showed significantly reduced responsiveness to LPS 3–60 days post-surgery.
- Kupffer cells from sham-operated rats responded normally to LPS.
- A transient increase in LPS sensitivity was observed in the first two days after splenectomy.
Conclusions:
- Splenectomy and the loss of splenic factors alter Kupffer cell responsiveness to septic stimuli.
- Reduced Kupffer cell sensitivity to LPS post-splenectomy may result from a loss of splenic lymphokine priming.
- This diminished responsiveness could contribute to the higher incidence of severe infections following splenectomy.