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Morphological and Compositional Analysis of Neutrophil Extracellular Traps Induced by Microbial and Chemical Stimuli
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Morphological and Compositional Analysis of Neutrophil Extracellular Traps Induced by Microbial and Chemical Stimuli

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Impairment of the host's antibacterial resistance by norepinephrine activated neutrophils

Yasuhiro Tsuda1, Makiko Kobayashi, David N Herndon

  • 1Department of Internal Medicine, The University of Texas Medical Branch, Galveston, TX 77555, USA.

Burns : Journal of the International Society for Burn Injuries
|October 5, 2007
PubMed

Insights

Systemic inflammatory response syndrome (SIRS) increases susceptibility to infections. Norepinephrine (NE) drives the generation of immunosuppressive neutrophils (PMN-II), which contribute to this heightened susceptibility in SIRS mice.

Area of Science:

  • Immunology
  • Sepsis Pathophysiology
  • Inflammatory Response

Background:

  • Systemic inflammatory response syndrome (SIRS) significantly elevates the risk of infectious complications in mice.
  • Polymorphonuclear neutrophils with immunosuppressive ability (PMN-II) are implicated in the increased susceptibility of SIRS mice to sepsis.
  • Elevated plasma norepinephrine (NE) levels are observed in SIRS mice.

Purpose of the Study:

  • To investigate the role of norepinephrine (NE) in the generation of PMN-II during SIRS.
  • To determine if NE influences the immunosuppressive properties of neutrophils.

Main Methods:

  • Comparison of PMN-II generation and function in SIRS mice versus normal mice treated with NE.
  • Analysis of cytokine production (CCL2, IL-10, CCL3, IL-12) by neutrophils from SIRS and NE-treated mice.
  • Assessment of susceptibility to sepsis following cecal-ligation and puncture (CLP) in mice inoculated with NE-treated PMN.

Main Results:

  • NE-treated normal mice exhibited increased susceptibility to CLP-induced sepsis, mirroring SIRS mice.
  • PMN-II from both SIRS mice and NE-treated PMN produced immunosuppressive biomarkers CCL2 and IL-10.
  • Immunostimulatory biomarkers CCL3 and IL-12 were absent in neutrophils from both groups.

Conclusions:

  • Massive NE production associated with SIRS plays a critical role in generating PMN-II.
  • The generated PMN-II are partially responsible for the increased susceptibility of SIRS mice to sepsis-induced infectious complications.

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