Traumatic injury often results in profound immunopathology that can lead to immunosuppression, thereby increasing the morbidity and mortality due to
sepsis. The isolation and partial characterization of an immunosuppressive
glycopeptide (SAP) from serum of severely burned patients has previously been reported by our laboratory. Recently, this
trauma peptide has also been identified in the serum of patients with multiple blunt
trauma. This
glycopeptide is capable of suppressing neutrophil chemotaxis, T-cell blastogenesis and the lysis of human erythrocytes. We demonstrate in this report that SAP inhibits
interleukin 2 (IL-2) biosynthesis by
mitogen-stimulated peripheral blood mononuclear cells.
Peptide concentrations of 50 nmol and above significantly inhibited
IL-2 production. Inhibition was not reduced by the addition of
indomethacin or anti-PGE2 to cultures containing greater than 100 nmol of
peptide, suggesting that inhibition is not entirely
prostaglandin-mediated. Preliminary studies have shown that
IL-2 suppression by SAP can be partially reversed by the addition of
calcium ionophore. These results suggest a potential immunosuppressive mechanism of the
trauma peptide in which T cell blastogenesis is inhibited by interference in
IL-2 biosynthesis.