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Related Experiment Videos

Cytokines, sepsis and immunomodulation

R G Molloy1, J A Mannick, M L Rodrick

  • 1Department of Surgical Immunology, Harvard Medical School, Boston, Massachusetts.

The British Journal of Surgery
|March 1, 1993
PubMed
Summary

Cytokines like tumor necrosis factor (TNF) and interleukins (IL) 1 and 6 mediate metabolic and immune changes during tissue injury and infection. Aberrant cytokine release can cause sepsis syndrome, prompting research into targeted therapies.

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Area of Science:

  • Immunology
  • Metabolic Medicine
  • Biochemistry

Background:

  • Tissue injury and infection disrupt host metabolic and immune balance.
  • Mononuclear phagocytes release endogenous mediators, including cytokines, that significantly influence these disruptions.
  • Key cytokines such as tumor necrosis factor (TNF) and interleukins (IL) 1 and 6 are central to the host response.

Purpose of the Study:

  • To review the role of cytokines in metabolic and immune alterations following tissue injury and infection.
  • To examine how these mediators contribute to the development of the sepsis syndrome.
  • To discuss novel therapeutic strategies targeting cytokine pathways.

Main Methods:

  • Review of existing scientific literature on cytokine involvement in trauma and sepsis.

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  • Analysis of the pathophysiological roles of TNF, IL-1, and IL-6.
  • Evaluation of emerging therapies aimed at modulating cytokine activity.

    • Main Results:

    • Cytokines orchestrate fuel substrate and hormonal adjustments crucial for host defense during trauma and sepsis.
    • Excessive release of TNF, IL-1, and IL-6 can lead to multi-organ dysfunction and the sepsis syndrome.
    • Therapies neutralizing endotoxin or blocking cytokines show promise for managing severe injury and infection.

    Conclusions:

    • Cytokines are critical effectors in the host response to injury and infection, influencing metabolic and immune homeostasis.
    • Dysregulated cytokine cascades, particularly in severe sepsis, precipitate multi-organ failure.
    • Targeted anti-cytokine therapies offer potential benefits but require rigorous clinical evaluation.