Role of fibroblast for eosinophilic airway inflammation

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Nasal polyposis and asthma are both manifestations of airway inflammatory diseases. Stromal abnormalities such as fibrosis, thickening of the basement membrane, and slughed-off epithelium with areas of epithelial metaplasia have been well described in varying degree, in both conditions. Fibroblasts are a rich source of cytokines and inflammatory cytokines and inflammatory mediators and are thought to play an important role in the development of fibrosis. In addition, there is considerable evidence for the participation of eosinophils in the pathophysiology of nasal polyps and asthma. Although increased numbers of eosinophils are present in nasal polyps and asthma, the mechanisms responsible for their selective accumulation are not completely clear. RANTES and eotaxin are chemokines that promote the recruitment of eosinophils. Thus, those may be important molecules for the recruitment of eosinophils in nasal polyps and asthma. Using primary airway tissue-derived fibroblast lines, we demonstrate that IL-1 and TNF induced the gene expression and protein production of RANTES and eotaxin in airway fibroblasts, and that LPS induced the gene expression and production of RANTES only in nasal but not in pharyngeal, tracheal, bronchial, and lung fibroblasts. These data suggest that airway fibroblasts may play an important role in the recruitment of eosinophils in airway diseases.