Nasal polyposis is a multifactorial disease with a strong inflammatory component. Its pathogenesis is often associated with ROS production catalysed by redox-active iron. This study aimed to characterize the roles of iron homeostasis and redox status in the pathogenesis of polyposis. Nasal polyps (NP) from asthmatics and non-asthmatics and turbinates from controls and NP-patients were analysed for ferritin, ferritin-bound iron (FBI) and levels of methionine-centred redox cycle proteins. The ferritin content in both NPs was significantly higher than in adjacent turbinates. No differences in FBI were observed between both NP groups and both turbinates groups, while in NPs it was significantly higher. In NP-turbinates the highest levels of redox proteins were observed. In conclusion, re-distribution of iron occurs upon the development of NP. While FBI is elevated in NPs, the adjacent turbinate remain iron-poor and low-inflammatory, suggesting the formation of virtual boundary between these tissues.
Bibliographical noteFunding Information:
This study was supported by research grants from Dr Avraham Moshe and Pepka Bergman Memorial Fund, from the Israel Science Foundation (316/05) and from Joels Landovsky Fund at the Hebrew University of Jerusalem. M. Chevion is the incumbent of the Dr William Chair of Heart Studies at the Hebrew University of Jerusalem. No competing financial interests exist.
- methionine-centred redox cycle
- nasal polyposis