OBJECTIVE: IL-18 expression and functional activity has been identified in several autoimmune and infectious diseases. To clarify the potential role of IL-18 during pulmonary Behçet's disease (BD), we have explored the capacity of IL-18 to induce the expression of IFN-gamma. METHODS: We studied bronchoalveolar lavage (BAL) from 12 patients with BD, 10 patients with silicosis as the control disease and 10 BAL from healthy subjects. BAL fluid, and BAL fluid cell cultures were investigated for IL-18 estimation by ELISA. Analysis of IL-18 and IFN-gamma gene expression was carried out before and after LPS stimulation. RESULTS: BD patients had significantly elevated levels of IL-18 in BAL fluid compared with control disease and healthy subjects. Induction of IFN-gamma and IL-18 were observed from BD-BAL fluid cells both spontaneously and after LPS stimulation, at higher levels compared to silicosis patients and healthy subjects (HC). Spontaneously only BD BAL cells expressed IL-18 mRNA and IFN-gamma mRNA. Forty-eight hours after LPS stimulation IL-18 mRNA and IFN-gamma mRNA were observed in BD, silicosis and HC cells. Recombinant IL-18 induced IFN-gamma production in BD- BAL fluid cells. CONCLUSION: Administration of IL-18 induced greater IFN-gamma production in BD-BAL fluid cells, than in normal BAL fluid cells. Our data indicate that IL-18 up-regulation is a feature of BD and suggest that IL-18 and IFN-gamma may contribute to the local inflammatory response in BD.
OBJECTIVE:IL-18 expression and functional activity has been identified in several autoimmune and infectious diseases. To clarify the potential role of IL-18 during pulmonary Behçet's disease (BD), we have explored the capacity of IL-18 to induce the expression of IFN-gamma. METHODS: We studied bronchoalveolar lavage (BAL) from 12 patients with BD, 10 patients with silicosis as the control disease and 10 BAL from healthy subjects. BAL fluid, and BAL fluid cell cultures were investigated for IL-18 estimation by ELISA. Analysis of IL-18 and IFN-gamma gene expression was carried out before and after LPS stimulation. RESULTS: BD patients had significantly elevated levels of IL-18 in BAL fluid compared with control disease and healthy subjects. Induction of IFN-gamma and IL-18 were observed from BD-BAL fluid cells both spontaneously and after LPS stimulation, at higher levels compared to silicosispatients and healthy subjects (HC). Spontaneously only BD BAL cells expressed IL-18 mRNA and IFN-gamma mRNA. Forty-eight hours after LPS stimulation IL-18 mRNA and IFN-gamma mRNA were observed in BD, silicosis and HC cells. Recombinant IL-18 induced IFN-gamma production in BD- BAL fluid cells. CONCLUSION: Administration of IL-18 induced greater IFN-gamma production in BD-BAL fluid cells, than in normal BAL fluid cells. Our data indicate that IL-18 up-regulation is a feature of BD and suggest that IL-18 and IFN-gamma may contribute to the local inflammatory response in BD.
Authors: H Nagafuchi; M Takeno; H Yoshikawa; M S Kurokawa; K Nara; E Takada; C Masuda; M Mizoguchi; N Suzuki Journal: Clin Exp Immunol Date: 2005-02 Impact factor: 4.330