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Phospholipase A2 is a circulating mediator in typhoid fever
M Keuter1, E Dharmana, B J Kullberg
1Department of Medicine, University Hospital Nijmegen, Utrecht University, Netherlands.
The Journal of Infectious Diseases
|July 1, 1995
Summary
Elevated levels of extracellular phospholipase A2 (PLA2) were found in typhoid fever patients, suggesting it may mediate disease symptoms. Levels decreased significantly after treatment, indicating PLA2
Area of Science:
- Immunology
- Infectious Diseases
- Biochemistry
Background:
- Typhoid fever presents as a systemic disease with prolonged fever, yet specific proinflammatory mediators were previously unidentified.
- Extracellular phospholipase A2 (group II, 14-kDa), induced by cytokines like IL-1 and TNF, is a potential mediator of inflammatory effects.
Purpose of the Study:
- To investigate the role of circulating extracellular phospholipase A2 (PLA2) as a potential mediator in typhoid fever patients.
- To quantify PLA2 concentrations in typhoid fever patients during illness and recovery.
Main Methods:
- Measurement of circulating PLA2 concentrations in 12 typhoid fever patients upon admission and at various follow-up points, including after recovery.
- Assessment of PLA2 levels in relation to disease severity (complicated vs. uncomplicated).
- Investigation of PLA2 production in lipopolysaccharide-stimulated whole blood cultures.
Main Results:
- Mean PLA2 concentrations were significantly elevated in typhoid fever patients upon admission (1444 +/- 1560 ng/mL).
- PLA2 levels decreased significantly by day 14 of recovery (55 +/- 48 ng/mL).
- Patients with complicated typhoid fever exhibited higher PLA2 levels on admission compared to those with uncomplicated disease.
- PLA2 was not detected in lipopolysaccharide-stimulated whole blood cultures, suggesting extra-corporeal cellular origin.
Conclusions:
- Circulating extracellular phospholipase A2 (PLA2) is elevated in typhoid fever and may act as a mediator of the disease's inflammatory processes.
- The reduction in PLA2 levels post-treatment correlates with clinical improvement.
- PLA2 likely originates from non-blood cells, highlighting its systemic role in protracted inflammatory conditions like typhoid fever.