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The role of neutrophils in severe sepsis

José C Alves-Filho, Andressa de Freitas, Fernando Spiller

    Shock (Augusta, Ga.)
    |August 16, 2008
    PubMed

    Insights

    Neutrophil migration failure in sepsis leads to more bacteria and reduced survival. This impairment is linked to excessive nitric oxide (NO) production, hindering immune response.

    Area of Science:

    • Immunology
    • Cell Biology
    • Pathophysiology

    Background:

    • Neutrophils are crucial for innate immunity, and their impaired migration to infection sites correlates with poor sepsis outcomes.
    • Severe sepsis is characterized by a failure of neutrophil migration, leading to increased bacterial load and decreased survival rates.
    • Neutrophils from septic patients show reduced chemotaxis compared to healthy individuals.

    Discussion:

    • Systemic Toll-like receptor activation by bacterial products triggers excessive cytokine/chemokine release in sepsis.
    • These mediators, along with LPS, induce inducible nitric oxide synthase (iNOS), leading to high nitric oxide (NO) levels.
    • NO impairs neutrophil migration by reducing CXCR2 expression and adhesion molecule levels, diminishing leukocyte-endothelial interactions.

    Key Insights:

    • Nitric oxide (NO) is a key mediator of neutrophil migration failure in severe sepsis.
    • NO-induced reduction in CXCR2 and adhesion molecules disrupts neutrophil chemotaxis and endothelium-leukocyte interactions.
    • Peroxynitrite contributes to the NO-mediated impairment of neutrophil function.

    Outlook:

    • Further research is needed to fully elucidate the complex mechanisms of neutrophil migration failure in sepsis.
    • Understanding these pathways could lead to novel therapeutic strategies to restore neutrophil function and improve sepsis outcomes.
    • Targeting NO production or its downstream effects may represent a promising approach for sepsis treatment.

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