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Targeting neutrophils in sepsis
Fabiane Sônego1, José Carlos Alves-Filho, Fernando Queiróz Cunha
1Department of Pharmacology, Ribeirão Preto Medical School, University of São Paulo, Ribeirão Preto, São Paulo, Brazil.
Expert Review of Clinical Immunology
|May 29, 2014
Summary
Neutrophil recruitment is reduced in severe sepsis due to receptor changes, impacting infection control and organ damage. Understanding these neutrophil roles in sepsis offers potential therapeutic targets.
Area of Science:
- Immunology
- Pathophysiology
- Critical Care Medicine
Background:
- Sepsis presents a significant global health challenge with high mortality rates.
- The complex pathophysiology of sepsis hinders comprehensive understanding and effective treatment development.
- Neutrophils are crucial for infection control, but their recruitment is impaired in severe sepsis.
Purpose of the Study:
- To review recent advancements in understanding neutrophil roles during sepsis.
- To highlight neutrophils as a potential therapeutic target for sepsis.
Main Methods:
- Review of current literature on neutrophil function in sepsis.
- Analysis of molecular mechanisms affecting neutrophil recruitment (e.g., receptor expression).
Main Results:
- Severe sepsis reduces neutrophil recruitment to infection sites via CXCR2 down-regulation.
- Toll-like receptor activation, TNF-α, and nitric oxide contribute to reduced neutrophil recruitment.
- CCR2 expression on neutrophils post-sepsis induction facilitates recruitment to distant organs, causing damage.
Conclusions:
- Neutrophil dysfunction is a key feature of severe sepsis.
- Altered neutrophil trafficking and function contribute to both infection persistence and organ injury.
- Targeting neutrophil behavior presents a promising avenue for sepsis therapy.
