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128. Kongress der Deutschen Gesellschaft für Chirurgie

Deutsche Gesellschaft für Chirurgie

03.05. - 06.05.2011, München

Platelet associated chemokines are increased during experimental colitis

Meeting Abstract

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  • Larissa Sachs - Uniklinik Münster, Allgemein- und Viszeralchirurgie, Münster

Deutsche Gesellschaft für Chirurgie. 128. Kongress der Deutschen Gesellschaft für Chirurgie. München, 03.-06.05.2011. Düsseldorf: German Medical Science GMS Publishing House; 2011. Doc11dgch074

doi: 10.3205/11dgch074, urn:nbn:de:0183-11dgch0747

Published: May 20, 2011

© 2011 Sachs.
This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( You are free: to Share – to copy, distribute and transmit the work, provided the original author and source are credited.



Introduction: There is growing recognition of cross-talk between platelets and leukocytes during inflammatory bowel disease. Recent findings implicate that the recruitment of platelets into the inflamed tissue could be mediated by the expression and secretion of chemokines. Aims of the present study were to define of the roles of the chemokine ligands and receptors SDF-1α/CXCR4 and CX3CL1 (fractalkine)/CX3CR1 in a murine model of experimental colitis.

Materials and methods: Colitis was induced in wild type (WT) C57Bl/6J mice with 3% dextran sulphate sodium (DSS) in drinking water for 7 days (DSS, n=6). Control mice received water (n=4). Severity of colitis was assessed daily using clinical parameters (Disease Activity Index (DAI) and a histologic damage score. Besides H&E –histology and immunofluorescence (IF) staining for the chemokines SDF-1α, CXCR4, fractalkine and CX3CR1, ELISA was performed in blood samples for these chemokines after 2, 4 and 7 days of DSS feeding. For statistical analysis Scheffe and student’s t-test were used (p<0.05).

Results: Compared with healthy control mice DSS-treated animals showed a significant increase in the DAI (0 vs 3,4 ± 0,37, p<0,05). H&E staining revealed intense infiltrates of inflammatory cells in all layers in mice treated with DSS. Semi-quantitative analysis of IF staining demonstrated an increased expression of fractalkine and its receptor CX3CR1, but not of SDF-1α und CXCR4, in colonic tissues of DSS treated mice in comparison with untreated animals. ELISA showed a significant increase of fractalkine after 4 and 7 days and SDF-1α after 7 days of DSS-induced colitis compared with healthy controls.

Conclusion: Our findings implicate a role for fractalkine, CX3CR1 and SDF-1α in the pathogenesis of DSS-induced colitis. This suggests that 1. the recruitment of platelets is governed by fractalkine and CXC3CR1 interaction and that 2. platelets contribute to sustaining the inflammatory response. (Supported by DFG VO 998/3-1)