• Shock · Dec 2012

    Follistatin does not influence the course of Escherichia coli K1 sepsis in a mouse model.

    • Wolfgang Brück, Catharina Dieelberg, Sandra Ribes, Uwe Michel, Sandra Redlich, Roland Nau, and Sandra Schütze.
    • Institute of Neuropathology, University Medical Center Göttingen, Germany.
    • Shock. 2012 Dec 1;38(6):615-9.

    AbstractFollistatin (FS) is the binding protein of activin A and inhibits its actions. The activin/FS system participates in the fine tuning of the immune response, and concentrations of activin A and FS are elevated in serum of patients with sepsis. Intraperitoneal injection of FS markedly reduced mortality after lipopolysaccharide-induced inflammation in a mouse model. Here, we investigated whether FS also influences the disease course in a mouse model of sepsis induced by intraperitoneal injection of Escherichia coli K1, a gram-negative bacterium frequently causing septic bacterial infections. Intraperitoneal injection of 10 μg/mL FS 30 min before infection did not influence survival, weight, motor performance, or bacterial titers of the infected mice. Thus, we could not confirm the protective effect of FS observed during lipopolysaccharide-induced inflammation in our mouse model of E. coli sepsis. Although it is a promising therapeutic tool in chronic or acute inflammatory conditions not caused by virulent pathogens, FS does not seem to increase the resistance to bacterial infections.

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