AJP - Lung Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
QUICK SEARCH:   [advanced]


     

Am J Physiol Lung Cell Mol Physiol (March 25, 2005). doi:10.1152/ajplung.00380.2004
This Article
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
289/2/L280    most recent
00380.2004v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Nakatani-Okuda, A.
Right arrow Articles by Okamura, H.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Nakatani-Okuda, A.
Right arrow Articles by Okamura, H.
Submitted on October 12, 2004
Accepted on March 21, 2005

Protection against bleomycin-induced lung injury by IL-18 in mice

Akemi Nakatani-Okuda1, Haruyasu Ueda2, Shin-ichiro Kashiwamura2, Atsuo Sekiyama2, Akira Kubota3, Yukihisa Fujita4, Susumu Adachi5, Yoshiyuki Tsuji5, Takakuni Tanizawa6, and Haruki Okamura2*

1 Department of Pediatrics, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan; Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
2 Institute for Advanced Medical Sciences, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
3 Department of Surgical Pathology, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
4 Department of Medical Physicochemistry, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
5 Department of Gynecology, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan
6 Department of Pediatrics, Hyogo College of Medicine, Nishinomiya, Hyogo, Japan

* To whom correspondence should be addressed. E-mail: haruoka{at}hyo-med.ac.jp.

Role of interleukin (IL) -18 in the protection from interstitial pneumonia and pulmonary fibrosis induced by Bleomycin (BLM) was investigated by comparing the severity of BLM-induced lung injuries between wild- type and C57BL/6 mice with a targeted knockout mutation of the IL-18 gene (IL-18 -/- mice). IL-18 -/- mice showed much worse lung injuries than wild-type mice, as assessed by the survival rate, histological images, leukocyte infiltration in the bronchoalveolar lavage fluid (BALF) and myeloperoxidase activity. In wild-type mice, administration of IL-18 prior to BLM instillation resulted in suppression of lung injuries, increases in the hydroxyproline content and decreases in the granulocyte-macrophage colony-stimulating factor (GM-CSF) content in the lung. Pre-administration of IL-18 also resulted in prevention of the reduction of the lung IL-10 content caused by BLM-induced damage of alveolar epithelial. BLM instillation suppressed superoxide dismutase (SOD) activity in IL-18 -/- mice to a greater extent than in wild-type mice. Pre-treatment of IL-18 augmented Mn-containing superoxide dismutase (Mn-SOD) messenger RNA expression and SOD activity in the lung and prevented the reduction of SOD activity caused by BLM in both wild-type and IL-18 -/- mice. These results suggest that IL-18 plays a protective role against BLM-induced lung injuries by up-regulating a defensive molecule, Mn-SOD.




This article has been cited by other articles:


Home page
 JEMHome page
H.-R. Kang, C. G. Lee, R. J. Homer, and J. A. Elias
Semaphorin 7A plays a critical role in TGF-{beta}1-induced pulmonary fibrosis
J. Exp. Med., May 14, 2007; 204(5): 1083 - 1093.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH
Visit Other APS Journals Online
Copyright © 2005 by the American Physiological Society.