Topic
Radiation-induced lung injury
About: Radiation-induced lung injury is a research topic. Over the lifetime, 258 publications have been published within this topic receiving 6877 citations. The topic is also known as: Radiation Pneumonitis.
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TL;DR: How PET-based novel quantitative techniques can be used to detect pulmonary and cardiovascular complications of radiation therapy earlier than current imaging modalities or clinical presentation allow is discussed.
Abstract: Radiation-induced normal tissue toxicities vary in terms of pathophysiologic determinants and timing of disease development, and they are influenced by the dose and radiation volume the critical organs receive, and the radiosensitivity of normal tissues and their baseline rate of cell turnover. Radiation-induced lung injury is dose limiting for the treatment of lung and thoracic cancers and can lead to fibrosis and potentially fatal pneumonitis. This article focuses on pulmonary and cardiovascular complications of radiation therapy and discusses how PET-based novel quantitative techniques can be used to detect these events earlier than current imaging modalities or clinical presentation allow.
2 citations
2 citations
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TL;DR: SBRT for lung cancer patients was safe, the majority of late RIL was mass-like pattern, which was difficult to be distinguished from tumor progression, which leaded to misdiagnosis of 24.5% patients receiving SBRT.
2 citations
TL;DR: MiR-223 effectively reduces the secretion of radiation- induced inflammatory factors IL-1β and IL-18 by inhibiting the expression of NLRP3 in lung tissue of mice, and thus has protective effect on radiation-induced lung injury.
Abstract: Objective
To investigate the radioprotective function and its mechanism of miR-223 in acute radiation-induced lung injury in mice.
Methods
Forty female C57BL/6 J mice were randomly divided into healthy control group, irradiation group, irradiation plus miR-223 group and irradiation plus NC group. Radiation groups were exposed with a single dose of 15 Gy of 6 MV X-rays delivered by a linear accelerator. The mice in drug group were administered by tail vein injection with miR-223 agomir or agomir-NC every other day from 1 d before irradiation to 14 d after irradiation. The lung tissue samples of mice were taken at 14 d post-irradiation. The pathological changes were observed by HE staining. The localization and expressions of IL-1β and IL-18 were observed by immunohistochemistry (IHC). Real-time PCR was used to detect miR-223, but NLRP3 mRNA expression in lung tissue. Western blot was used to detect the protein expressions of NLRP3 and Caspase-1, and ELISA assay was used to detect the expressions of IL-1β and IL-18 in lung homogenate.
Results
Radiation decreased the expression of miR-223, but increased the expression of NLRP3 in lung tissue. Administration of miR-223 agomir inhibited the expression of NLRP3 and attenuated lung inflammation. HE and IHC staining showed that miR-223 reduced the acute inflammatory response and the expressions of IL-1β and IL-18 in lung tissue compared with irradiation group (t=10.16, 6.00, P<0.05). The expressions of NLRP3 and Caspase-1 protein in lung tissue of irradiated plus miR-223 group was lower than that in the irradiation alone group (t=12.47, 4.95, P<0.05). ELISA assay also showed a decrease of inflammatory factors IL-1β and IL-18 in lung tissue homogenate of the irradiation plus miR-223 group (t=8.22, 8.47, P<0.05).
Conclusions
MiR-223 effectively reduces the secretion of radiation-induced inflammatory factors IL-1β and IL-18 by inhibiting the expression of NLRP3 in lung tissue of mice, and thus has protective effect on radiation-induced lung injury.
Key words:
miR-223; Radiation-induced lung injury; NLRP3
2 citations