Intercellular adhesion molecule 1 knockout abrogates radiation induced pulmonary inflammation

Hallahan, Dennis E.; Virudachalam, Subbulakshmi

doi:10.1073/pnas.94.12.6432

Cited by 154 publications

(76 citation statements)

References 34 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…40,41 It was also reported that acute respiratory distress syndrome caused by radiation was prevented by the use of anti-IL-8 antibody. 42,43 In conclusion, these findings suggest that intravenous injection of a sufficient number (10 7 ) of fully differentiated NB4 cells was necessary to cause RAS in NOD/scid mice. Administration of ATRA was also necessary.…”

Section: Figurementioning

confidence: 90%

Retinoic acid syndrome in NOD/scid mice induced by injecting an acute promyelocytic leukemia cell line

et al. 2004

View full text Add to dashboard Cite

All-trans retinoic acid (ATRA) induces complete remission in patients with acute promyelocytic leukemia (APL). However, ATRA sometimes causes retinoic acid syndrome (RAS) characterized by respiratory distress, pleural effusions, fever and weight gain. To investigate the pathophysiology of RAS, we generated an animal model by injecting an APL cell line, NB4, into immunodeficient mice. When NOD/scid mice were injected intravenously with fully differentiated NB4 cells (1 Â 10 7 ) and then given a daily administration of ATRA, three of 12 mice died of pulmonary edema within 14 days. Pathologically, dilated lung capillary vessels and alveolar effusions were observed. After the injection, NB4 cells were detected in the lung within 2 days and in the pleural effusion later on. The gene expression levels of CXC chemokines (MIP-2 and KC) and ICAM-1 were increased in the lung and heart by the ATRA administration. In immunohistochemical analyses, MIP-2 was clearly detected in alveolar macrophages of the lung in mice with RAS. Dexamethasone treatment prevented the development of RAS and decreased the CXC chemokine mRNA expression in the lung. These findings suggested that the activation of adhesion molecules for leukocytes and expression of CXC chemokines in the lung are closely involved in triggering RAS.

show abstract

Section: Figurementioning

confidence: 90%

Retinoic acid syndrome in NOD/scid mice induced by injecting an acute promyelocytic leukemia cell line

et al. 2004

View full text Add to dashboard Cite

show abstract

“…Late fibrosis might also develop months to years post-therapy. A possible contribution of cytokines and chemokines to the development of radiation-induced lung injury has been suggested [6][7][8][9][10]. The risk of radiation pneumonitis could also be strongly affected by various endogenous (genotypic) and exogenous (environmental) factors which vary among individuals [11].…”

Section: Introductionmentioning

confidence: 99%

High superoxide dismutase and low glutathione peroxidase activities in red blood cells predict susceptibility of lung cancer patients to radiation pneumonitis

Park

Ramnath

Yang

et al. 2007

Free Radical Biology and Medicine

View full text Add to dashboard Cite

Radiation pneumonitis is an unpredictable complication of radiotherapy for lung cancer and a condition which can cause significant morbidity. The ability to identify patients at a high risk of developing pneumonitis is critical, since it will enable the individualization of the treatment plan. Because the cytotoxic effect of radiation is propagated through ROS and ROS-driven oxidative stress, the role of anti-oxidant defense systems in radiation pneumonitis was investigated. Using the pneumonitis-sensitive C3H/HeN mice as a model, we demonstrated that the anti-oxidant response of the lung correlated well with that of RBC. We then proceeded to test whether differences of RBC anti-oxidant response would predict the pneumonitis development in patients. SOD, GPX, CAT activities and glutathione in RBC were measured at baseline and then weekly for 6 weeks of treatment in fifteen eligible patients receiving concurrent chemo-radiotherapy for unresectable stage III NSCLC. Striking differences were found in the anti-oxidant activities of RBC with respect to the pneumonitis development. Those who developed pneumonitis showed higher SOD and lower GPX activities at baseline compared to those who did not (3.7 vs. 6.8 unit/mg for median SOD, 16.5 vs. 10.7 nmol/min/mg for median GPX). The functional imbalance of SOD and GPX was displayed consistently throughout the treatment period. The sensitivity and specificity of pneumonitis prediction were further increased when the GPX/SOD ratio was analyzed (pre-treatment P = 0.0046). Our results provide a strong rationale to monitor SOD and GPX activities of RBC to identify patients who are at risk of developing pneumonitis, and to implement a strategy of increasing the GPX/SOD ratio in order to lower the risk.

show abstract

“…These doses were selected on the basis of evidence of stimulation of putative atherogenic events in isolated vascular cells and animal models, [32][33][34][35] without effects on vascular or endothelial integrity. In initial studies, we confirmed the latter by ascertaining that there were no significant changes in endothelial permeability based on Evans blue dye exclusion or uptake of 125 I-LDL for up to 10 days at any of the doses used (data not shown).…”

Section: Atherogenic Effects Of Ionizing Radiation In C57bl/6 Micementioning

confidence: 99%

Ionizing Radiation Accelerates Aortic Lesion Formation in Fat-Fed Mice via SOD-Inhibitable Processes

Tribble

Barcellos‐Hoff

Chu

et al. 1999

ATVB

View full text Add to dashboard Cite

Abstract-Ionizing radiation promotes formation of reactive oxygen species, including the superoxide anion (O 2 Ϫ ). To evaluate whether O 2 Ϫ or O 2 Ϫ -mediated perturbations may contribute to the known atherogenic effects of radiation, we examined aortic lesion formation in irradiated C57BL/6 mice and evaluated the effects of CuZn-superoxide dismutase (CuZn-SOD) overexpression. Ten-week-old mice were exposed to a 2-, 4-, or 8-Gy dose of 250-keV x-rays to the upper thorax and then placed on a high-fat diet for 18 weeks. Based on quantitative lipid staining of serial sections of the proximal aorta, mean lesion area was increased with increasing radiation dose and was 3-fold greater in 8-Gy-irradiated than sham-irradiated mice (7800Ϯ2140 versus 2635Ϯ709 m 2 , PϽ0.05). These effects were absolutely dependent on a high-fat diet, which had to be introduced within 1 to 2 weeks of the radiation exposure, suggesting the early involvement of atherogenic lipoproteins that were elevated in response to the diet. The importance of radiation-induced oxidative stress was supported by the observation of a 2-fold lower mean lesion area in irradiated CuZn-SOD transgenic mice than in their irradiated, nontransgenic littermates (3026Ϯ1590 versus 6102Ϯ1834 m 2 , PϽ0.05). Lucigeninenhanced chemiluminescence, used as an index of aortic O 2 Ϫ concentrations, was significantly elevated in the postradiation period, and this response was reduced in CuZn-SOD transgenics. On the basis of these results, we propose that radiation may be a useful tool for initiating oxidative or redox-regulated events that promote atherogenesis and for testing the antiatherogenic properties of antioxidants.

show abstract

Intercellular adhesion molecule 1 knockout abrogates radiation induced pulmonary inflammation

Cited by 154 publications

References 34 publications

Retinoic acid syndrome in NOD/scid mice induced by injecting an acute promyelocytic leukemia cell line

Retinoic acid syndrome in NOD/scid mice induced by injecting an acute promyelocytic leukemia cell line

High superoxide dismutase and low glutathione peroxidase activities in red blood cells predict susceptibility of lung cancer patients to radiation pneumonitis

Ionizing Radiation Accelerates Aortic Lesion Formation in Fat-Fed Mice via SOD-Inhibitable Processes

Contact Info

Product

Resources

About