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Related Experiment Video

Updated: Aug 6, 2025

Intestinal Epithelial Regeneration in Response to Ionizing Irradiation

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Published on: July 27, 2022

Epithelial Responses in Radiation-Induced Lung Injury (RILI) Allow Chronic Inflammation and Fibrogenesis.

Tyler A Beach¹, Jacob N Finkelstein², Polly Y Chang¹

¹SRI Biosciences, SRI International, Menlo Park, Calfornia 94025-3493.

Radiation Research

|March 17, 2023

Summary

Radiation-induced lung injury (RILI) leads to fibrosis. This study reveals that lung epithelial cells

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Area of Science:

Radiation biology
Pulmonary medicine
Cell biology

Background:

Whole thorax lung irradiation (WTLI) causes progressive lung injury, often leading to irreversible radiation-induced pulmonary fibrosis (RIPF).
Resident pulmonary epithelial cells are crucial for lung homeostasis but can contribute to radiation-induced lung injury (RILI) progression.
Understanding the in vivo epithelial response to irradiation is key to developing therapeutic strategies.

Purpose of the Study:

To investigate the in vivo response of lung epithelium during the progression of radiation-induced pulmonary fibrosis (RIPF) using an unbiased RNA sequencing approach.
To identify specific molecular changes in lung epithelial cells following irradiation that contribute to RILI progression.

Main Methods:

Isolation of CD326+ epithelium from C57BL/6J mice subjected to 12.5 Gy WTLI.
RNA sequencing of irradiated and non-irradiated epithelial cells and whole lung tissue at regular intervals.
Validation of findings using quantitative PCR (qPCR) and immunohistochemistry.

Main Results:

Transcripts regulating immune responses and fibroblast activation were significantly reduced in irradiated lungs by 4 weeks post-irradiation.
Alveolar type-2 epithelial cells (AEC2) numbers decreased significantly post-irradiation, indicated by reduced pro-surfactant protein C (pro-SPC) expression.
Expression of Cd200 and cyclooxygenase 2 (COX2), which suppress immune and fibroblast activation, was reduced in CD326+ cells.

Conclusions:

Epithelial cell loss and reduced expression of immune/fibroblast regulatory molecules (Cd200, COX2) contribute to RILI progression and RIPF.
Strategies aimed at preventing epithelial cell loss or restoring epithelial-derived mediators may be effective for treating radiation-induced lung injury.