作者: David Préfontaine , Stéphane Lajoie-Kadoch , Susan Foley , Séverine Audusseau , Ron Olivenstein
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摘要: IL-33, a new member of the IL-1 cytokine family, promotes Th2 inflammation, but evidence on implications this in asthma is lacking. IL-33 would be mainly expressed by structural cells, whether proinflammatory cytokines modulate its expression airway smooth muscle cells (ASMC) unknown. Endobronchial biopsies were obtained from adults with mild (n = 8), moderate severe 9), and control subjects 5). Immunocytochemistry, laser-capture microdissection, reverse transcriptase, real-time quantitative PCR used for determining lung tissues. ASMC isolated resected specimens cultured dexamethasone. was determined PCR, ELISA, Western blotting. Higher levels transcripts are detected asthmatic compared subjects, especially asthma. show at both protein mRNA levels. TNF-alpha transcript correlate tissues, up-regulates time- dose-dependent manner. IFN-gamma also increases shows synergistic effect TNF-alpha. Dexamethasone fails to abolish TNF-alpha-induced up-regulation. bronchial controls, as well severity. source cytokine. Our data propose novel inflammatory marker refractory