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1 February 2006 Interleukin 1β (IL1B) Signaling is a Critical Component of Radiation-Induced Skin Fibrosis
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Abstract

Liu, W., Ding, I., Chen, K., Olschowka, J., Xu, J., Hu, D., Morrow, G. and Okunieff, P. Interleukin 1β (IL1B) Signaling is a Critical Component of Radiation-Induced Skin Fibrosis. Radiat. Res. 165, 181–191 (2006).

Interleukin 1 beta (IL1B), a potent pro-inflammatory cytokine, is directly up-regulated by radiation and is known to regulate other inflammation-related molecules, such as the matrix metalloproteinases (MMPs) and their endogenous inhibitors (TIMPs). However, the nature of the interaction of IL1B with MMPs and TIMPs in radiation-induced skin fibrosis is unknown. We examined the response of primary dermal keratinocytes, fibroblasts and endothelial cells to single-fraction radiation (10 Gy) and compared the results to a temporal sequence of histology from irradiated C57BL/6 and IL1R1 knockout mice. These studies showed that keratinocytes are the major IL1-producing cells in vitro and that radiation induces an immediate and chronic elevation in the expression of IL1B mRNA in the skin of C57BL/6 mice. This elevation was principally early and was less pronounced in the IL1R1 knockout strain, which also demonstrated reduced late radiation fibrosis. Radiation also increased expression of MMP mRNA in C57BL/6 mice. Finally, exogenous IL1B protein induced robust endogenous IL1B mRNA expression, along with a brisk increase in MMPs and collagen III, but only in the C57BL/6 mice. In conclusion, these data suggest that IL1B plays a critical role in radiation-induced fibrosis and that the increased MMPs fail to block the IL1-related collagen accumulation.

Weimin Liu, Ivan Ding, Keqiang Chen, John Olschowka, Jianhua Xu, Dongping Hu, Gary R. Morrow, and Paul Okunieff "Interleukin 1β (IL1B) Signaling is a Critical Component of Radiation-Induced Skin Fibrosis," Radiation Research 165(2), 181-191, (1 February 2006). https://doi.org/10.1667/RR3478.1
Received: 9 February 2005; Accepted: 1 August 2005; Published: 1 February 2006
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