Related Experiment Video
Updated: Jul 11, 2026

08:38
Using a Bacterial Pathogen to Probe for Cellular and Organismic-level Host Responses
Published on: February 22, 2019
Systemic and local high mobility group box 1 concentrations during severe infection
Marieke A D van Zoelen1, Pierre-François Laterre, Suzanne Q van Veen
1Center for Infection and Immunity Amsterdam, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands. M.A.vanZoelen@amc.uva.nl
Critical Care Medicine
|September 29, 2007
Summary
High mobility group box 1 (HMGB1) release kinetics in severe sepsis vary by infection source. HMGB1 concentrations are elevated at the infection site, suggesting localized release in pneumonia and peritonitis.
Area of Science:
- Sepsis pathophysiology
- Immunology
- Molecular biology
Background:
- High mobility group box 1 (HMGB1) is a known late mediator in sepsis.
- Understanding HMGB1 release patterns is crucial for sepsis management.
Purpose of the Study:
- To investigate HMGB1 release in sepsis patients stratified by common infectious sources.
- To quantify HMGB1 concentrations at infection sites in peritonitis and pneumonia.
Main Methods:
- Observational study involving sepsis patients and healthy volunteers.
- Measurement of HMGB1 and cytokine levels in plasma and at infection sites (abdominal fluid, bronchoalveolar lavage).
- Stratification of sepsis patients by infection source: pneumonia, peritonitis, and urinary tract infection.
Main Results:
- Elevated HMGB1 in sepsis due to pneumonia (days 0 and 3) and peritonitis (day 0).
- Delayed HMGB1 elevation in urinary tract infection (day 3).
- HMGB1 concentrations were significantly higher at the infection site (peritonitis, pneumonia) compared to plasma.
Conclusions:
- HMGB1 release kinetics in severe sepsis are dependent on the primary infection source.
- HMGB1 is likely released predominantly at the site of infection in severe cases.
Related Concept Videos
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...
Acute Inflammation II: Cellular Phase
The cellular phase of acute inflammation is a tightly orchestrated sequence of events that recruits leukocytes, primarily neutrophils, to sites of tissue injury or infection. Following the initial vascular changes, this phase ensures effective immune cell migration, activation, and function at the affected site to eliminate pathogens and initiate tissue repair.Leukocyte Recruitment CascadeLeukocyte recruitment happens in four steps: margination, adhesion, transmigration, and chemotaxis. Reduced...
