Related Experiment Video

Updated: Aug 17, 2026

Isolation and Chemical Characterization of Lipid A from Gram-negative Bacteria
12:57

Isolation and Chemical Characterization of Lipid A from Gram-negative Bacteria

Published on: September 17, 2013

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
PubMed

Insights

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.

More Related Videos

Isolation of Lipoprotein Particles from Chicken Egg Yolk for the Study of Bacterial Pathogen Fatty Acid Incorporation into Membrane Phospholipids11:59

Isolation of Lipoprotein Particles from Chicken Egg Yolk for the Study of Bacterial Pathogen Fatty Acid Incorporation into Membrane Phospholipids

Published on: May 15, 2019

A Liposome Membrane Permeability Assay for Investigating the Effects of Phosphatidylinositol Phosphate Groups on Membranotropic Action of Venom PLA210:31

A Liposome Membrane Permeability Assay for Investigating the Effects of Phosphatidylinositol Phosphate Groups on Membranotropic Action of Venom PLA2

Published on: September 26, 2025

Related Concept Videos

Phosphoinositides and PIPs01:42

Phosphoinositides and PIPs

Phosphoinositides are a group of phospholipids containing a glycerol backbone with two fatty acid chains and a phosphate attached to a myoinositol sugar ring. The inositol head group extends into the cytoplasm, where it is modified by adding phosphate groups to form phosphatidylinositol phosphates or PIPs.
Different phosphoinositides are synthesized and recruited on the cytosolic face of the plasma membrane. The localization of specific phosphoinositides concentrated in separate membrane...
IP3/DAG Signaling Pathway01:11

IP3/DAG Signaling Pathway

Membrane lipids such as phosphatidylinositol (PI) are precursors for several membrane-bound and soluble second messengers. Specific kinases phosphorylate PI and produce phosphorylated inositol phospholipids. One such inositol phospholipids are the  phosphatidylinositol-4,5 bisphosphate [PI(4,5)P2], present in the inner half of the lipid bilayer. Upon ligand binding, GPCR stimulates Gq proteins to turn on phospholipase Cꞵ. Activated phospholipase Cꞵ cleaves PI(4,5)P2 and produces two-second...
Formation of Lipopolysaccharides01:19

Formation of Lipopolysaccharides

Lipopolysaccharides (LPS) are crucial components of the outer membrane of Gram-negative bacteria, serving both structural and functional roles. It contributes to membrane stability and protects bacteria from host immune responses. LPS is composed of three major regions—lipid A, a core oligosaccharide, and an O antigen. The biosynthesis and assembly of LPS involve a highly coordinated set of enzymatic reactions and transport mechanisms. Additionally, LPS is recognized as an endotoxin, triggering...
Amebiasis01:28

Amebiasis

Entamoeba histolytica, a protozoan parasite, is responsible for intestinal and extraintestinal amebiasis. Though a significant proportion of infections remain asymptomatic, approximately 50 million individuals annually are estimated to present with clinical disease, resulting in up to 100,000 deaths globally. The disease burden is disproportionately high in regions with lower socioeconomic status, such as parts of India, Africa, Mexico, and Latin America.Etiology and TransmissionThe infective...
Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Gastritis II: Pathophysiology01:26

Gastritis II: Pathophysiology

The pathophysiology of gastritis begins with the colonization of the stomach lining by Helicobacter pylori (H. pylori). This bacterium spreads mainly via the oral-oral route through saliva or shared utensils, and can also be transmitted in overcrowded or unhygienic environments through contaminated water, despite its brief survival outside the body.ColonizationOnce ingested, H. pylori enters the stomach and begins colonization by navigating through the mucus layer lining the stomach wall. It...