Artikel
Decreased expression of PSGL-1 is another sign for the global anti-inflammatory phenotype of circulating monocytes in GBM patients
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Autoren
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Sascha Marx
- Universitätsmedizin Greifswald, Klinik und Poliklinik für Neurochirurgie, Greifswald, Deutschland
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Frederik Kinnen
- Universitätsmedizin Greifswald, Klinik und Poliklinik für Neurochirurgie, Greifswald, Deutschland
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Sebastian Paul
- Universitätsmedizin Greifswald, Klinik und Poliklinik für Augenheilkunde, Greifswald, Deutschland
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Sandra Bien-Möller
- Universitätsmedizin Greifswald, Institut für Pharmakologie, Greifswald, Deutschland
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Bernhard Rauch
- Universitätsmedizin Greifswald, Institut für Pharmakologie, Greifswald, Deutschland
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Christoph A. Ritter
- Ernst Moritz Arndt Universität, Department of clinical pharmacy, Greifswald, Deutschland
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Henry W. S. Schroeder
- Universitätsmedizin Greifswald, Klinik und Poliklinik für Neurochirurgie, Greifswald, Deutschland
| Veröffentlicht: | 18. Juni 2018 |
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Gliederung
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Objective: Despite the activation status of circulating platelets was increased in GBM patients, the formation of platelet-monocyte conjugates was rather decreased in previous experiments of our group. PSGL-1, a surface receptor on monocytes, is a key player in the interaction with platelets. The aim of the present study was to determine the PSGL-1 expression as well as the expression of different M1/ M2 markers on the surface of circulating monocytes in GBM patients.
Methods: Blood samples of 11 consecutive patients with GBM and 11 age- and gender matched healthy controls were drawn from an antecubital vein prior to tumor surgery. The expression of PSGL-1, CD163, CD204, CD169, HLA-ABC and HLA-DR on monocytes was determined by flow cytometry.
Results: The mean age of GBM patients was 65 years (range from 48 to 86 years). No differences were seen between groups with regard to previous medication and medical history, except that 8/ 11 GBM patients received dexamethasone in the days prior to blood sampling.
PSGL-1 expression was significantly reduced on monocytes of GBM patients (MFI: 77.7 vs. 111.7; p=0.04). CD163 expression was significantly increased on monocytes of GBM patients (MFI: 56 vs. 14.8; p=0.01). CD204 expression was rather increased on monocytes of GBM patients, but the expression itself was very low. There were no differences between both groups in the expression of CD169. Both, HLA-ABC and HLA-DR expression was significantly reduced on monocytes of GBM-patients (HLA-ABC MFI: 34.2 vs. 92.8; p=0.01 and HLA-DR MFI: 20.5 versus 118; p=0.0006).
The findings did not correlate with the cumulative dose of dexamethasone given in the days prior to blood sampling. However, HLA-DR and CD163 expression were not different in the 3 GBM patients without dexamethasone compared to their healthy controls. The reduced PSGL-1 expression on circulating monocytes of GBM patients was completely independent of dexamethasone medication.
Conclusion: The present study shows for the first time a decreased expression of PSGL-1 on circulating monocytes in GBM patients. This is a proper explanation for the rather decreased formation of platelet-monocyte conjugates, which we could show in previous experiments, and might be another sign for an anti-inflammatory phenotype of circulating monocytes in GBM patients. Interestingly, the changes of CD163 and HLA-DR expression on monocytes in GBM patients are mainly due to dexamethasone medication in the present study.
