Rhinology · 2006
Eosinophilic nasal polyps are a rich source of eotaxin, eotaxin-2 and eotaxin-3.
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Olze H, Förster U, Zuberbier T, Morawietz L, Luger E O
Аннотация
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.
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.