作者: Gerrit John , Shashi Chillappagari , Bruce K. Rubin , Dieter C. Gruenert , Markus O. Henke
DOI: 10.3109/01902148.2011.569968
关键词:
摘要: ABSTRACTAs part of the innate and adaptive immune system, airway epithelial cells secrete proinflammatory cytokines after activation Toll-like receptors (TLRs) by pathogens. Nevertheless, cystic fibrosis (CF) airways are chronically infected with Pseudomonas aeruginosa, suggesting a modified response in CF. The authors have shown that CF bronchial cells, reduced surface expression TLR-4 causes diminished interleukin (IL)-8 IL-6 upon lipopolysaccharide (LPS) stimulation. However, there is no information regarding MyD88 (myeloid differentiation primary gene 88)-independent signaling pathway LPS, which results responses secretion T cell–recruiting chemokine interferon-γ–inducible protein (IP)-10. Therefore, investigated induction IP-10 cell line CFBE41o− its CFTR-corrected isotype under well-differentiating conditions. e...