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P- and E-selectin blockade can control bacterial translocation and modulate systemic inflammatory response

Francisco J García-Criado1, Francisco S Lozano, Marcello B Barros

  • 1Department of Surgery, Clinic Hospital and University of Salamanca, Salamanca, Spain. marcellobb@bol.com.br

Journal of Investigative Surgery : the Official Journal of the Academy of Surgical Research
|August 30, 2005
PubMed

Insights

GM 1998-016, a novel compound, effectively reduced bacterial translocation in rats by inhibiting inflammatory responses and leukocyte-endothelium interactions. This finding suggests a potential therapeutic strategy for managing sepsis and multi-organ failure.

Area of Science:

  • Immunology
  • Microbiology
  • Pharmacology

Background:

  • Bacterial translocation contributes to sepsis and organ failure.
  • Selectins mediate leukocyte-endothelium interactions crucial in inflammation.
  • Targeting selectins may modulate inflammatory responses and bacterial translocation.

Purpose of the Study:

  • To evaluate the efficacy of GM 1998-016, a Sialyl-Lewis(X) derivative, in modulating bacterial translocation.
  • To investigate the compound's impact on systemic inflammation and leukocyte-endothelium interactions.
  • To assess the protective effects of GM 1998-016 in an in vivo model.

Main Methods:

  • Wistar rats were administered Zymosan A and treated with varying doses of GM 1998-016.
  • Bacterial translocation (local and systemic) was quantified.
  • Neutrophil infiltration, oxidative stress markers, and cytokine levels were measured.

Main Results:

  • GM 1998-016 significantly decreased bacterial translocation (p < .05).
  • The compound reduced neutrophil infiltration (p < .001), free radical production (p < .01), and pro-inflammatory cytokines (p < .01).
  • GM 1998-016 effectively downregulated systemic inflammation and leukocyte-endothelium interactions.

Conclusions:

  • GM 1998-016 demonstrates significant protective effects against bacterial translocation in an experimental model.
  • The compound acts by downregulating inflammatory responses and leukocyte-endothelium interactions.
  • GM 1998-016 shows promise as a therapeutic agent for conditions involving bacterial translocation and inflammation.

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