Abstract
The present investigation using Positron Emission Tomography shows how peptide VSAK can reduce the detrimental effects produced by lipopolysaccharides in Dutch dwarf rabbits, used to develop the Systemic Inflammatory Response Syndrome (SIRS). Animals concomitantly treated with lipopolysaccharides (LPS) and peptide VSAK show important protection in the loss of radiolabeled-glucose uptake observed in diverse organs when animals are exclusively treated with LPS. Treatment with peptide VSAK prevented the onset of changes in serum levels of glucose and insulin associated with the establishment of SIRS and the insulin resistance-like syndrome. Treatment with peptide VSAK also allowed an important attenuation in the circulating levels of pro-inflammatory molecules in LPS-treated animals. As a whole, our data suggest that peptide VSAK might be considered as a candidate in the development of new therapeutic possibilities focused on mitigating the harmful effects produced by lipopolysaccharides during the course of SIRS.
Highlights
The present investigation using Positron Emission Tomography shows how peptide VSAK can reduce the detrimental effects produced by lipopolysaccharides in Dutch dwarf rabbits, used to develop the Systemic Inflammatory Response Syndrome (SIRS)
Employing a synthetic peptide containing 18 amino acids derived from this carboxy-end segment of cholesterol-ester transfer protein intestinal isoform (CETPI), we have described that the interaction between peptide VSAK and LPS can neutralize LPS induced toxicity in vitro as well as in vivo
Peptide VSAK prevents the deleterious effects of circulating LPS allowing a normal tissue [18F] FDG permeation in a model of the systemic inflammatory response syndrome
Summary
The present investigation using Positron Emission Tomography shows how peptide VSAK can reduce the detrimental effects produced by lipopolysaccharides in Dutch dwarf rabbits, used to develop the Systemic Inflammatory Response Syndrome (SIRS). Sepsis is characterized by the presence of infection in association with a dysregulated host response and organ failure; while, septic shock includes the development of systemic h ypotension[3,4] Dysregulation of this response is mainly characterized by an imbalance in the systems that regulate the host’s immune activation when the presence of the pathogen leads to the development of a hyper-inflammatory state followed by the exhaustion of the immune system to adequately r espond[5]. Lipid A considered the most conserved region of LPS, presents special importance for recognition by the immune system When this region binds to a member of the lipopolysaccharide-binding protein family, the complex is recognized by the TLR4 receptor, and the development of the host response initiates[13]
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