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Updated: Jun 5, 2026
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Design of Cecal Ligation and Puncture and Intranasal Infection Dual Model of Sepsis-Induced Immunosuppression
Published on: June 15, 2019
[Pathophysiological basis of surgery-linked sepsis].
1Institut für Experimentelle Chirurgie, Medizinische Fakultät, Universität Rostock, Schillingallee 69a, Rostock, Germany. brigitte.vollmar@med.uni-rostock.de
Der Chirurg; Zeitschrift Fur Alle Gebiete Der Operativen Medizen
|January 21, 2011
Summary
Injury and infection trigger inflammatory responses. Sepsis progresses from inflammation to immunosuppression, increasing infection risk and organ damage. Understanding these immune shifts aids new therapeutic development.
Area of Science:
- Immunology
- Pathophysiology
- Sepsis Research
Context:
- Infection and injury initiate host inflammatory responses.
- Pattern recognition receptors (PRRs) recognize pathogen-associated molecular patterns (PAMPs) and damage-associated molecular patterns (DAMPs).
- Dysregulated inflammation contributes to significant morbidity and mortality.
Purpose:
- To explore the complex immune response to infection and injury.
- To understand the progression of sepsis from hyperinflammation to immunosuppression.
- To identify key mediators and mechanisms driving sepsis pathophysiology.
Summary:
- Sepsis involves a shift from initial hyperinflammation to immunosuppression, impairing pathogen clearance and increasing secondary infection risk.
- Immune suppression in sepsis is linked to lymphocyte depletion, reduced HLA-DR expression, and a shift towards anti-inflammatory Th2 cells.
- Key sepsis mediators include HMGB1, MIF, and complement factor C5a, with amplified coagulation and inflammation cascades.
Impact:
- Identifies central pathomechanistic events in sepsis, including immune dysbalance and neuroimmunomodulation.
- Highlights the potential for developing novel therapeutics targeting the systemic host response.
- Provides insights into modulating, rather than inhibiting, the immune response to infection and trauma.
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