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Obesity exacerbates sepsis-induced inflammation and microvascular dysfunction in mouse brain
Vidula Vachharajani1, Janice M Russell, Keith L Scott
1Department of Critical Care Medicine, Louisiana State University Health Sciences Center, Shreveport 71130-3932, USA.
Microcirculation (New York, N.Y. : 1994)
|April 15, 2005
Summary
Obesity exacerbates sepsis-induced inflammation and thrombosis in the brain
Area of Science:
- Immunology
- Pathophysiology
- Vascular Biology
Background:
- Obesity is linked to increased sepsis morbidity and mortality.
- Mechanisms underlying this disparity remain unclear.
Purpose of the Study:
- To investigate inflammatory and thrombogenic responses in the cerebral microvasculature of obese versus lean mice during sepsis.
Main Methods:
- Cecal ligation and perforation model in obese and lean wild-type mice.
- Measurement of leukocyte and platelet adhesion, behavioral responses, and P-selectin expression.
- Evaluation of immunoblockade effects on adhesion molecule pathways.
Main Results:
- Obese mice showed exaggerated proinflammatory and prothrombogenic cerebral microvascular responses to sepsis.
- Blocking P-selectin, ICAM-1, or CD18 attenuated these enhanced responses.
- Obese mice exhibited greater sepsis-induced behavioral deficits and P-selectin expression.
Conclusions:
- Exaggerated microvascular inflammation and thrombosis, involving endothelial cell activation and adhesion molecule expression (e.g., P-selectin), contribute to increased sepsis morbidity in obesity.