%0 Journal Article
%T Modulation of neutrophil function by the tripeptide feG
%A Ronald D Mathison
%A A Befus
%A Joseph S Davison
%A Richard C Woodman
%J BMC Immunology
%D 2003
%I BioMed Central
%R 10.1186/1471-2172-4-3
%X With human neutrophils feG had no discernible effect on oxidative burst or phagocytosis, but in picomolar amounts it reduced PAF-induced neutrophil movement and adhesion, and the binding of CD11b by 34% and that of CD16b close to control values. In the rat feG (10-11M) reduced the binding of CD11b and CD16 antibodies to PAF-stimulated circulating neutrophils by 35% and 43%, respectively, and at 100 micrograms/kilograms intraperitoneally feG reduced neutrophil in vivo migration by 40%. With ovalbumin-sensitized rats that were challenged with antigen, feG inhibited binding of antibodies against CD16b but not CD11b, on peritoneal leukocytes.The inhibitory effect of feG on neutrophil movement may be mediated by alterations in the co-stimulatory molecules CD11b and CD16.The VCS-1 gene encodes a multipotent prohormone as a 146 amino acid protein named SMR1 [1]. From proximal N-terminal dibasic cleavage sites a pentapeptide, QHNPR, is generated that is involved in the modulation of mineral balance [2], whereas from the carboxyl-terminus a 7 amino acid peptide (TDIFEGG; SGP-T) is an inhibitor of endotoxic hypotension [3] and intestinal anaphylaxis [4]. This heptapeptide can be shortened to a biologically active pentapeptide (FEGGG) or tripeptide (FEG) [4]. The conversion of the tripeptide into its D-isomeric form (feG) favors its oral administration, yielding a significant reduction in anaphylactic responses of the intestine, heart and lungs [5,6]. The anti-inflammatory effects of these salivary gland peptides have been postulated in animal models to be due to the inhibitory effects on neutrophil chemotaxis [7,8] and leukocyte rolling [9], although relatively little is known of the effects of these peptides on human neutrophils.Neutrophils participate in the first line of defense against potentially harmful microorganisms [10,11], but they also contribute to the underlying pathology associated with acute lung [12], ischemia-reperfusion [13] and burn [14] injuries, arthritis
%U http://www.biomedcentral.com/1471-2172/4/3