Eosinophil Infiltration Mechanisms in Chronic Rhinosinusitis

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  • Ohori Junichiro
    Kagoshima University Graduate School of Medical and Dental Sciences
  • Kurono Yuichi
    Kagoshima University Graduate School of Medical and Dental Sciences

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  • 好酸球性副鼻腔炎における好酸球浸潤の機序
  • コウサンキュウセイ フクビクウエン ニ オケル コウサンキュウ シンジュン ノ キジョ

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Abstract

Eosinophilic chronic rhinosinusitis (ECRS) symptoms include massive eosinophilic infiltration into nasal mucosa, nasal polyps, and curative resistance even postoperatively. How so many eosinophils migrate into nasal tissues is unclear, although infiltration is associated with intractability. Two factors considered potentially related are (1) increased eosinophils infiltration from blood vessels into tissue and (2) eosinophil “pools” in tissue due to age. During adherence in local eosinophil infiltration, vascular cell adhesion molecules (VCAM)-1 and alpha 4 beta 1 integrin (VLA-4) bind eosinophils selectivery. Tumor necrosis factor (TNF)-a or interleukin (IL)-4 stimulation increases VCAM-1 expression in vascular endothelial cells, multiplying nasal polyp fibroblasts. This, in turn, stimulates eosinophil infiltration. Eotaxin, a chemokine involved in eosinophil chemotaxis, is expressed significantly more highly in nasal polyp fibroblasts from those with ECRS in TNF-α and IL-4 costimulation than in those without ECRS. mRNA expression of IL-5, a cytokine important in eosinophil survival, is high in the nasal polyps of those with ECRS. The expression of tumor necrosis-factor-related apoptosis-inducing ligand (TRAIL), associated with eosinophil apoptosis, does not differ between those with and without ECRS, whereas that of TRAIL-R3 in peripheral blood eosinophils is higher in those with ECRS. High TRAIL-R3 expression suppresses eosinophil apoptosis. The above factors are, however, associated only partially with eosinophil infiltration, meaning that the mechanism must be further analyzed to clarify ECRS features and determine safe, effective treatment.<br>

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