title: Knockdown of Myeloid Differentiation Factor 88 Attenuates Lipopolysaccharide-Induced Inflammatory Response in Pancreatic Ductal Cells.
abstract: OBJECTIVE
  The aim of the study was to explore the potential role of myeloid differentiation factor 88 (MyD88), which acts as an adaptor in the TLR4 signalling pathway, in immune responses of the pancreatic duct during acute pancreatitis.
  
  
  METHODS
  Primary cultures of pancreatic duct epithelial cells from Wistar rats and cultures of the pancreatic ductal ARIP cell line were treated with lipopolysaccharide (LPS), and expression of toll-like receptor 4 mRNA was determined using real-time PCR, expression of MyD88 protein using Western blot, and levels of inflammatory cytokines using enzyme-linked immunosorbent assay. These experiments were repeated using ARIP cells in which MyD88 expression was stably knocked down.
  
  
  RESULTS
  Toll-like receptor 4 and MyD88 expression were similar between pancreatic duct epithelial cells and ARIP cells after LPS stimulation. Myeloid differentiation factor 88 knockdown led to significantly lower levels of inflammatory cytokines after LPS induction in ARIP cells.
  
  
  CONCLUSIONS
  Myeloid differentiation factor 88 knockdown attenuates LPS-induced inflammatory responses in pancreatic ductal cells, suggesting that the MyD88 pathway plays a critical role in their immune defense activity.
authors.affiliation: From the *Institute of Digestive Surgery and State Key Laboratory of Biotherapy, and †Department of Gastroenterological Surgery, West China Hospital, Sichuan University, Sichuan, People's Republic of China.
authors.forename: Yong
authors.initials: Y
authors.lastname: Liu
authors.forename: Yang
authors.initials: Y
authors.lastname: Li
authors.forename: Ke-Ling
authors.initials: KL
authors.lastname: Chen
authors.forename: Bin
authors.initials: B
authors.lastname: Zhou
authors.forename: Zhao-Yin
authors.initials: ZY
authors.lastname: Lv
authors.forename: Zong-Guang
authors.initials: ZG
authors.lastname: Zhou
authors.forename: Yuan
authors.initials: Y
authors.lastname: Li
mesh_terms: D000818:Animals; D015153:Blotting, Western; D002460:Cell Line; D002478:Cells, Cultured; D016207:Cytokines / Q000235:genetics* / Q000378:metabolism; D004797:Enzyme-Linked Immunosorbent Assay; D004847:Epithelial Cells / Q000187:drug effects / Q000378:metabolism; D015870:Gene Expression / Q000187:drug effects; D018836:Inflammation Mediators / Q000378:metabolism; D016753:Interleukin-10 / Q000235:genetics / Q000378:metabolism; D015850:Interleukin-6 / Q000235:genetics / Q000378:metabolism; D008070:Lipopolysaccharides / Q000494:pharmacology*; D008856:Microscopy, Fluorescence; D053594:Myeloid Differentiation Factor 88 / Q000235:genetics* / Q000378:metabolism; D010183:Pancreatic Ducts / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D034622:RNA Interference; D017208:Rats, Wistar; D020133:Reverse Transcriptase Polymerase Chain Reaction; D051197:Toll-Like Receptor 4 / Q000235:genetics / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics / Q000378:metabolism
chemical_list: D016207:Cytokines; D018836:Inflammation Mediators; D015850:Interleukin-6; D008070:Lipopolysaccharides; D053594:Myeloid Differentiation Factor 88; D051197:Toll-Like Receptor 4; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10