help button home button Am J Pathol R & D Systems
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS

This Article
Right arrow Order Full text via Infotrieve
Services
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
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Smith, D. R.
Right arrow Articles by Gilbert, A. R.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Smith, D. R.
Right arrow Articles by Gilbert, A. R.

American Journal of Pathology, Vol 143, 794-803, Copyright © 1993 by American Society for Investigative Pathology

REGULAR ARTICLES

The production of interleukin-1 receptor antagonist by human bronchogenic carcinoma

DR Smith, SL Kunkel, TJ Standiford, SW Chensue, MW Rolfe, MB Orringer, RI Whyte, MD Burdick, JM Danforth and AR Gilbert
Department of Medicine, University of Michigan Medical School, Ann Arbor 48109-0360.

Bronchogenic carcinoma displays an aggressive clinical course that may reflect a capacity to evade host defenses. We postulated that tumors may elaborate interleukin-1 receptor antagonist protein (IRAP) to escape host interleukin-1-dependent responses. Homogenates of human bronchogenic lung tumors demonstrated significant increases of IRAP compared with normal lung tissue controls (n = 48). There was no significant difference in interleukin-1 beta levels between tumor and normal lung tissue. Immunohistochemical staining localized IRAP to tumor cells. Semiquantitative pathological analysis demonstrated a modest inflammatory cell infiltrate with qualitative differences between tumors of different histology. Western blot analysis of tumor homogenates demonstrated several molecular weight forms of IRAP. Finally, antigenic IRAP was detected in supernatants of the human bronchogenic carcinoma cell line (A549) maintained in vitro. These findings illustrate the capacity of bronchogenic tumors to produce and secrete IRAP that may be important in tumor evasion of host defenses.


This article has been cited by other articles:


Home page
 Am. J. Respir. Cell Mol. Bio.Home page
Y. A. Schwarz, R. S. Amin, J. M. Stark, B. C. Trapnell, and R. W. Wilmott
Interleukin-1 Receptor Antagonist Inhibits Interleukin-8 Expression in A549 Respiratory Epithelial Cells Infected In Vitro with a Replication-Deficient Recombinant Adenovirus Vector
Am. J. Respir. Cell Mol. Biol., September 1, 1999; 21(3): 388 - 394.
[Abstract] [Full Text]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1993 by the American Society for Investigative Pathology.