These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.
Pubmed for Handhelds
PUBMED FOR HANDHELDS
Search MEDLINE/PubMed
Title: Eosinophilic nasal polyps are a rich source of eotaxin, eotaxin-2 and eotaxin-3. Author: Olze H, Förster U, Zuberbier T, Morawietz L, Luger EO. Journal: Rhinology; 2006 Jun; 44(2):145-50. PubMed ID: 16792175. Abstract: INTRODUCTION: The CC-chemokine eotaxin plays a key role in the pathologic mechanism of tissue eosinophilia in nasal polyposis. In this study, we investigated a possible role of eotaxin-2 and eotaxin-3, the recently discovered members of the eotaxin family. METHODS: Nasal polyps from 24 patients (non allergic/allergic/aspirin-intolerant patients) and turbinate tissue from 8 controls were investigated. Chemokine protein content (eotaxin, eotaxin-2, and -3) of tissue homogenates was measured by ELISA. Paraffin sections of samples were stained to determine the extent of eosinophilia. RESULTS: Protein expression of eotaxin, eotaxin-2 and eotaxin-3 was significantly higher in nasal polyps than in controls. There was a direct correlation between the protein concentrations of all three eotaxins. Further, protein levels of all chemokines were significantly correlated to the amount of eosinophilia. In aspirin-sensitive polyps the number of eosinophils was significantly higher than in the other patient groups and they had significantly higher eotaxin, eotaxin-2, and -3 protein levels than non-allergic and significantly higher amounts of eotaxin-3 compared with allergic patients. CONCLUSIONS: Our findings suggest, that all members of the eotaxin family are involved in the pathogenesis of nasal polyposis. The results are more likely indicative of a complex cooperation between all members of the eotaxin family than of a specific role in the development of eosinophilia and nasal polyposis.[Abstract] [Full Text] [Related] [New Search]