作者: S. Kusaka , A. Nishida , K. Takahashi , S. Bamba , H. Yasui
DOI: 10.1111/CEI.13047
关键词: Interferon 、 Molecular biology 、 Inflammatory bowel disease 、 Lipopolysaccharide 、 Immunology 、 Messenger RNA 、 Biology 、 TRIF 、 Transforming growth factor 、 Kinase 、 Small interfering RNA
摘要: Cathelicidin peptide LL-37 plays an important role in the early host response against invading pathogens via its broad-spectrum anti-microbial activity. In this study, we investigated expression inflamed mucosa of inflammatory bowel disease (IBD) patients. Furthermore, regulatory mechanism induction was human colonic subepithelial myofibroblasts (SEMFs). mRNA and protein secretion were analysed using real-time polymerase chain reaction enzyme-linked immunosorbent assay, respectively. Intracellular signalling pathways immunoblotting specific small interference RNA (siRNA). The increased significantly ulcerative colitis Crohn's disease. Toll-like receptor (TLR)-3 ligand, polyinosinic-polycytidylic acid (poly(I:C), induced stimulated SEMFs. transfection siRNAs for intracellular proteins [Toll/IL-1R domain-containing adaptor-inducing interferon (IFN) (TRIF), tumour necrosis factor receptor-associated (TRAF)6, transforming growth β-activated kinase (TAK)1] suppressed poly(I:C)-induced significantly. Poly(I:C)-induced phosphorylation mitogen-activated kinases (MAPKs) activated nuclear kappa B (NF-κB) activating (AP)-1. NF-κB c-Jun inhibited expression. lipopolysaccharide (LPS)-induced interleukin (IL)-6 IL-8 up-regulated IBD by TLR-3 stimulation exhibited effect interaction with (LPS).