| Outline of Final Research Achievements |
In this study, it has been shown that cytokine production in epithelial cells is enhanced and collagen production in fibroblasts is suppressed in a low zinc environment. These factors may contribute to the pathogenesis of sinusitis, particularly CRSwNP, and could be potential therapeutic targets. Gene expression of zinc transporters and zinc chelators was also examined, but expression was unaltered except for metallosionin, an intracellular chelator of zinc. qPCR and fluorescence immunostaining were used to examine tissue zinc and metallosionin expression in vivo and in vitro, and results showed that sinusitis in sinusitis, metallothionein was considered to be a consequence rather than a cause of low zinc. These decreased tissue zinc level, epithelium-derived cytokines, collagen and zinc homeostasis components may contribute to the pathogenesis of sinusitis, particularly CRSwNP, and may be useful as therapeutic targets.
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