Journal
AUTOIMMUNITY
Volume 46, Issue 5, Pages 323-328Publisher
TAYLOR & FRANCIS LTD
DOI: 10.3109/08916934.2012.747522
Keywords
low dose ionizing irradiation; anti-inflammation; macrophages; radiosensitivity; Balb/c mice; C57BL/6 mice; hTNF-tg mice
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Funding
- European Commissions (DoReMi, European Network of Excellence) [249689]
- German Federal Ministry of Education and Research (BMBF
- GREWIS) [02NUK017G]
- Interdisciplinary Center for Clinical Research (IZKF) at the University Hospital of the University of Erlangen-Nuremberg [A41]
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Since the beginning of the 20th century, low dose radiotherapy (LD-RT) has been practiced and established as therapy of inflammatory diseases. Several clinical studies already have proven the anti-inflammatory effect of low doses of ionizing irradiation (LDR). However, further research is inevitable to reveal the underlying immune-biological mechanisms. Focus has been set on the modulation of activated macrophages by LDR, since they participate in both, initiation and resolution of inflammation. Here we examined with an ex vivo peritoneal mouse macrophage model how LDR modulates the secretion of the inflammatory cytokines IL-1 beta and TNF-alpha by activated macrophages and whether the basal radiosensitivity of the immune cells has influence on it. Peritoneal macrophages of Balb/c mice responded to exposure of 0.5 or 0.7 Gy of ionizing irradiation (X-ray) with significant decreased release of IL-1 beta and slightly, but not significantly, reduced release of TNF-alpha. Macrophages of the less radiosensitive C57BL/6 mice did not show this anti-inflammatory reaction. This was observed in both wild type and human TNF-alpha transgenic animals with C57BL/6 background. We conclude that only the inflammatory phenotype of more radiosensitive macrophages is reduced by LDR and that ex vivo and in vivo models with primary cells should be applied to examine how the immune system is modulated by LDR.
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