Expression of Human Cathelicidin Peptide LL-37 in Inflammatory Bowel Disease.

作者: S. Kusaka , A. Nishida , K. Takahashi , S. Bamba , H. Yasui

DOI: 10.1111/CEI.13047

关键词: InterferonMolecular biologyInflammatory bowel diseaseLipopolysaccharideImmunologyMessenger RNABiologyTRIFTransforming growth factorKinaseSmall 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).

参考文章(37)
William R. Best, Jack M. Becktel, John W. Singleton, Rederived values of the eight coefficients of the Crohn's Disease Activity Index (CDAI). Gastroenterology. ,vol. 77, pp. 843- 846 ,(1979) , 10.1016/0016-5085(79)90384-6
Neeloffer Mookherjee, Kelly L Brown, Dawn ME Bowdish, Silvana Doria, Reza Falsafi, Karsten Hokamp, Fiona M Roche, Ruixia Mu, Gregory H Doho, Jelena Pistolic, Jon-Paul Powers, Jenny Bryan, Fiona SL Brinkman, Robert EW Hancock, None, Modulation of the TLR-Mediated Inflammatory Response by the Endogenous Human Host Defense Peptide LL-37 Journal of Immunology. ,vol. 176, pp. 2455- 2464 ,(2006) , 10.4049/JIMMUNOL.176.4.2455
Isao Nagaoka, Satoko Hirota, François Niyonsaba, Michimasa Hirata, Yoshiyuki Adachi, Hiroshi Tamura, Didier Heumann, Cathelicidin Family of Antibacterial Peptides CAP18 and CAP11 Inhibit the Expression of TNF-α by Blocking the Binding of LPS to CD14+Cells The Journal of Immunology. ,vol. 167, pp. 3329- 3338 ,(2001) , 10.4049/JIMMUNOL.167.6.3329
Lioba F. Courth, Maureen J. Ostaff, Daniela Mailänder-Sánchez, Nisar P. Malek, Eduard F. Stange, Jan Wehkamp, Crohn's disease-derived monocytes fail to induce Paneth cell defensins Proceedings of the National Academy of Sciences. ,vol. 112, pp. 14000- 14005 ,(2015) , 10.1073/PNAS.1510084112
M Sun, C He, Y Cong, Z Liu, Regulatory immune cells in regulation of intestinal inflammatory response to microbiota Mucosal Immunology. ,vol. 8, pp. 969- 978 ,(2015) , 10.1038/MI.2015.49
R. Bals, J. M. Wilson, Cathelicidins--a family of multifunctional antimicrobial peptides. Cellular and Molecular Life Sciences. ,vol. 60, pp. 711- 720 ,(2003) , 10.1007/S00018-003-2186-9
Kenshi Yamasaki, Jürgen Schauber, Alvin Coda, Henry Lin, Robert A. Dorschner, Norman M. Schechter, Chrystelle Bonnart, Pascal Descargues, Alain Hovnanian, Richard L. Gallo, Kallikrein-mediated proteolysis regulates the antimicrobial effects of cathelicidins in skin The FASEB Journal. ,vol. 20, pp. 2068- 2080 ,(2006) , 10.1096/FJ.06-6075COM
Ling C. Huang, Rose Y. Reins, Richard L. Gallo, Alison M. McDermott, Cathelicidin-deficient (Cnlp -/- ) mice show increased susceptibility to Pseudomonas aeruginosa keratitis. Investigative Ophthalmology & Visual Science. ,vol. 48, pp. 4498- 4508 ,(2007) , 10.1167/IOVS.07-0274
Ana Gutiérrez, Ernst Holler, Pedro Zapater, Laura Sempere, Rodrigo Jover, Miguel Pérez-Mateo, Juergen Schoelmerich, José Such, Reiner Wiest, Rubén Francés, Antimicrobial peptide response to blood translocation of bacterial DNA in Crohn's disease is affected by NOD2/CARD15 genotype. Inflammatory Bowel Diseases. ,vol. 17, pp. 1641- 1650 ,(2011) , 10.1002/IBD.21537