Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Sep 6:9:877.
doi: 10.3389/fonc.2019.00877. eCollection 2019.

Radiation-Induced Lung Injury (RILI)

Lorena Giuranno  1 , Jonathan Ient  1 , Dirk De Ruysscher  1 , Marc A Vooijs  1
Affiliations
Review

Radiation-Induced Lung Injury (RILI)

Lorena Giuranno et al. Front Oncol. .

Abstract

Radiation pneumonitis (RP) and radiation fibrosis (RF) are two dose-limiting toxicities of radiotherapy (RT), especially for lung, and esophageal cancer. It occurs in 5-20% of patients and limits the maximum dose that can be delivered, reducing tumor control probability (TCP) and may lead to dyspnea, lung fibrosis, and impaired quality of life. Both physical and biological factors determine the normal tissue complication probability (NTCP) by Radiotherapy. A better understanding of the pathophysiological sequence of radiation-induced lung injury (RILI) and the intrinsic, environmental and treatment-related factors may aid in the prevention, and better management of radiation-induced lung damage. In this review, we summarize our current understanding of the pathological and molecular consequences of lung exposure to ionizing radiation, and pharmaceutical interventions that may be beneficial in the prevention or curtailment of RILI, and therefore enable a more durable therapeutic tumor response.

Keywords: RILI; RILT; adverse effects; fibrosis; lung; pneumonitis; radiotherapy.

PubMed Disclaimer

Figures

Figure 1
Figure 1
Radiation-Induced Lung Injury (RILI). Schematic overview of the important steps leading to pulmonary toxicity after radiotherapy. Radiation induces reactive oxygen and nitrogen species (ROS, NGS) which leads to DNA strand breaks and to epithelial cell death. Inflammatory cells infiltrate the affected region to remove death cells. Leucocytes and lymphocytes proliferate and produce cytokines and chemokines, leading to an inflammatory condition highly deregulated in duration and perpetuation. The persistence of the inflammatory state culminates in early reversible toxicity (pneumonitis) and can develop in to irreversible late toxicity (fibrosis).
See this image and copyright information in PMC

Similar articles

See all similar articles

Cited by

See all "Cited by" articles

References

    1. Trott KR, Herrmann T, Kasper M. Target cells in radiation pneumopathy. Int J Radiat Oncol Biol Phys. (2004) 58:463–9. 10.1016/j.ijrobp.2003.09.045 - DOI - PubMed
    1. Wirsdorfer F, Jendrossek V. The role of lymphocytes in radiotherapy-induced adverse late effects in the lung. Front Immunol. (2016) 7:591. 10.3389/fimmu.2016.00591 - DOI - PMC - PubMed
    1. Azzam EI, Jay-Gerin JP, Pain D. Ionizing radiation-induced metabolic oxidative stress and prolonged cell injury. Cancer Lett. (2012) 327:48–60. 10.1016/j.canlet.2011.12.012 - DOI - PMC - PubMed
    1. Jack CI, Cottier B, Jackson MJ, Cassapi L, Fraser WD, Hind CR. Indicators of free radical activity in patients developing radiation pneumonitis. Int J Radiat Oncol Biol Phys. (1996) 34:149–54. 10.1016/0360-3016(95)00209-X - DOI - PubMed
    1. Tak JK, Park J-W. The use of ebselen for radioprotection in cultured cells and mice. Free Rad Biol Med. (2009) 46:1177–85. 10.1016/j.freeradbiomed.2009.01.023 - DOI - PubMed

LinkOut - more resources