期刊论文详细信息
BMC Immunology
Modulation of neutrophil function by the tripeptide feG
Richard C Woodman1  Joseph S Davison2  A Dean Befus3  Ronald D Mathison2 
[1] Ortho Biotech, 430 Route 22 East, Bridgewater, NJ 08807-0914, USA;Department of Physiology and Biophysics, Faculty of Medicine, University of Calgary, Calgary, Alberta, T2N 4N1, Canada;Department of Medicine, Faculty of Medicine and Dentistry, University of Alberta, Edmonton, Alberta, T6G 2S2, Canada
Others  :  1078429
DOI  :  10.1186/1471-2172-4-3
 received in 2002-11-01, accepted in 2003-03-04,  发布年份 2003
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【 摘 要 】

Background

Neutrophils are critical in the defense against potentially harmful microorganisms, but their excessive and inappropriate activation can contribute significantly to tissue damage and a worsening pathology. Through the release of endocrine factors submandibular glands contribute to achieving a balance in neutrophil function by modulating the state of activation and migratory potential of circulating neutrophils. A putative hormonal candidate for these effects on neutrophils was identified as a heptapeptide named submandibular gland peptide T (SGP-T; sequence = TDIFEGG). Since the tripeptide FEG, derived from SGP-T, and its D-amino acid analogue feG had similar inhibitory effects on inflammatory reactions, we investigated the effects of feG on human and rat neutrophil function.

Results

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.

Conclusions

The inhibitory effect of feG on neutrophil movement may be mediated by alterations in the co-stimulatory molecules CD11b and CD16.

【 授权许可】

   
2003 Mathison et al; licensee BioMed Central Ltd. This is an Open Access article: verbatim copying and redistribution of this article are permitted in all media for any purpose, provided this notice is preserved along with the article's original URL.

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