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[Cancer Research 57, 2096-2099, June 1, 1997]
© 1997 American Association for Cancer Research

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Ionizing Radiation Mediates Expression of Cell Adhesion Molecules in Distinct Histological Patterns within the Lung1

Dennis E. Hallahan2 and Subbulakshmi Virudachalam

Department of Radiation and Cellular Oncology, University of Chicago and Pritzker School of Medicine, Chicago, Illinois 60637

Inflammatory cell infiltration of the lung is a predominant histopathological change that occurs during radiation pneumonitis. Emigration of inflammatory cells from the circulation requires the interaction between cell adhesion molecules on the vascular endothelium and molecules on the surface of leukocytes. We studied the immunohistochemical pattern of expression of cell adhesion molecules in lungs from mice treated with thoracic irradiation. After X-irradiation, the endothelial leukocyte adhesion molecule 1 (ELAM-1; E-selectin) was primarily expressed in the pulmonary endothelium of larger vessels and minimally in the microvascular endothelium. Conversely, the intercellular adhesion molecule 1 (ICAM-1; CD54) was expressed in the pulmonary capillary endothelium and minimally in the endothelium of larger vessels. Radiation-mediated E-selectin expression was first observed at 6 h, whereas ICAM-1 expression initially increased at 24 h after irradiation. ICAM-1 and E-selectin expression persisted for several days. P-selectin is constitutively expressed in Weibel-Palade bodies in the endothelium, which moved to the vascular lumen within 30 min after irradiation. P-selectin was not detected in the pulmonary endothelium at 6 h after irradiation. The radiation dose required for increased cell adhesion molecule expression within the pulmonary vascular endothelium was 2 Gy, and expression increased in a dose-dependent manner. These data demonstrate that ICAM-1 and E-selectin expression is increased in the pulmonary endothelium following thoracic irradiation. The pattern of expression of E-selectin, P-selectin, and ICAM-1 is distinct from one another.

1 This work was funded by NIH Grant CA58508, the American Cancer Society, the Chicago Tumor Institute, Cancer Research Center, and the Center for Radiation Oncology.

2 To whom requests for reprints should be addressed, at Department of Radiation Oncology MC 0085, University of Chicago, 5841 South Maryland, Chicago, IL 60637. Phone: (773) 702-2526; Fax: (773) 702-4079; E-mail: hallahan@rover.uchicago.edu.

Received 2/12/97. Accepted 4/13/97.




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Copyright © 1997 by the American Association for Cancer Research.