Skip Navigation

This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
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 ISI Web of Science
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (6)
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Cale, C. M.
Right arrow Articles by Woolf, A. S.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Cale, C. M.
Right arrow Articles by Woolf, A. S.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nephrol Dial Transplant (2000) 15: 173-183
© 2000 European Renal Association-European Dialysis and Transplant Association

Inflammatory mediators in human renal dysplasia

Catherine M. Cale1, Nigel J. Klein2, Paul J. D. Winyard1 and Adrian S. Woolf1

1 Nephrourology Unit and 2 Immunobiology Unit, Institute of Child Health, UCLMS, London, UK

Correspondence and offprint requests to: Dr Catherine Cale, Department of Clinical Immunology, Great Ormond Street Hospital for Children NHS Trust, Great Ormond Street, London WC1N 3JH, UK.

Background. Cytokines regulate many processes in the immune system and have recently been implicated in normal organogenesis. We previously demonstrated that the archetypal inflammatory cytokine tumour necrosis factor-{alpha} (TNF-{alpha}) is expressed in the murine metanephros, and exogenous TNF-{alpha} inhibits nephrogenesis and increases macrophage numbers in vitro (Cale et al., Int J Dev Biol 1998; 42: 663–674). The phenotype seen, with an arrest of ureteric bud branching and failure of mesenchymal to epithelial conversion, is similar to human renal dysplasia.

Methods and results. In normal human fetal kidneys we demonstrated the presence of macrophages and T cells and also documented TNF receptor expression on ureteric bud derivatives. In contrast to normal tissues, TNF-{alpha} protein was detected in dysplastic kidneys. This factor was also detected in the urine of fetuses with obstructive uropathy and TNF receptors were expressed in dysplastic tubules. Furthermore, we noted a fetal distribution of macrophages and T cells in dysplastic tissues and persistent expression of the adhesion molecules neural cell adhesion molecule and intercellular adhesion molecule.

Conclusions. We suggest that abnormal expression of cytokines early in renal development dysregulates normal patterns of adhesion molecule expression and inflammatory cells, and may contribute to the pathogenesis of renal dysplasia.

Keywords: ICAM-1; macrophage; NCAM; renal dysplasia; TNF-{alpha}


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
 Am. J. Pathol.Home page
S. P. Yang, A. S. Woolf, H. T. Yuan, R. J. Scott, R. A. Risdon, M. J. O'Hare, and P. J. D. Winyard
Potential Biological Role of Transforming Growth Factor-{beta}1 in Human Congenital Kidney Malformations
Am. J. Pathol., November 1, 2000; 157(5): 1633 - 1647.
[Abstract] [Full Text] [PDF]


Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.