It appears you don't have support to open PDFs in this web browser. To view this file, Open with your PDF reader
Abstract
Shiga-toxigenic Escherichia coli (STEC) infection causes severe bloody diarrhea, renal failure, and hemolytic uremic syndrome. Recent studies showed global increases in Locus for Enterocyte Effacement (LEE)-negative STEC infection. Some LEE-negative STEC produce Subtilase cytotoxin (SubAB), which cleaves endoplasmic reticulum (ER) chaperone protein BiP, inducing ER stress and apoptotic cell death. In this study, we report that SubAB induces expression of a novel form of Lipocalin-2 (LCN2), and describe its biological activity and effects on apoptotic cell death. SubAB induced expression of a novel LCN2, which was regulated by PRKR-like endoplasmic reticulum kinase via the C/EBP homologous protein pathway. SubAB-induced novel-sized LCN2 was not secreted into the culture supernatant. Increased intracellular iron level by addition of holo-transferrin or FeCl3 suppressed SubAB-induced PARP cleavage. Normal-sized FLAG-tagged LCN2 suppressed STEC growth, but this effect was not seen in the presence of SubAB- or tunicamycin-induced unglycosylated FLAG-tagged LCN2. Our study demonstrates that SubAB-induced novel-sized LCN2 does not have anti-STEC activity, suggesting that SubAB plays a crucial role in the survival of LEE-negative STEC as well as inducing apoptosis of the host cells.
You have requested "on-the-fly" machine translation of selected content from our databases. This functionality is provided solely for your convenience and is in no way intended to replace human translation. Show full disclaimer
Neither ProQuest nor its licensors make any representations or warranties with respect to the translations. The translations are automatically generated "AS IS" and "AS AVAILABLE" and are not retained in our systems. PROQUEST AND ITS LICENSORS SPECIFICALLY DISCLAIM ANY AND ALL EXPRESS OR IMPLIED WARRANTIES, INCLUDING WITHOUT LIMITATION, ANY WARRANTIES FOR AVAILABILITY, ACCURACY, TIMELINESS, COMPLETENESS, NON-INFRINGMENT, MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE. Your use of the translations is subject to all use restrictions contained in your Electronic Products License Agreement and by using the translation functionality you agree to forgo any and all claims against ProQuest or its licensors for your use of the translation functionality and any output derived there from. Hide full disclaimer
Details
1 Chiba University, Department of Molecular Infectiology, Graduate School of Medicine, Chiba, Japan (GRID:grid.136304.3) (ISNI:0000 0004 0370 1101)
2 Kanazawa University, Advanced Health Care Science Research Unit, Institute for Frontier Science Initiative, Kanazawa, Japan (GRID:grid.9707.9) (ISNI:0000 0001 2308 3329)
3 Chiba University, Division of Molecular Immunology, Medical Mycology Research Center, Chiba, Japan (GRID:grid.136304.3) (ISNI:0000 0004 0370 1101); The University of Tokyo, Division of Mucosal Symbiosis, International Research and Development Center for Mucosal Vaccines, Institute of Medical Science, Tokyo, Japan (GRID:grid.26999.3d) (ISNI:0000 0001 2151 536X); AMED-PRIME, Japan Agency for Medical Research and Development, Tokyo, Japan (GRID:grid.480536.c) (ISNI:0000 0004 5373 4593)
4 National Institute of Infectious Diseases, Department of Bacteriology I, Tokyo, Japan (GRID:grid.410795.e) (ISNI:0000 0001 2220 1880)
5 Chiba University, Reproductive Medicine, Graduate School of Medicine, Chiba, Japan (GRID:grid.136304.3) (ISNI:0000 0004 0370 1101)
6 University of Tsukuba Hospital, Clinical Laboratory, Tsukuba, Japan (GRID:grid.412814.a) (ISNI:0000 0004 0619 0044)
7 National Institutes of Health, Pulmonary Branch, National Heart, Lung, and Blood Institute, Bethesda, USA (GRID:grid.94365.3d) (ISNI:0000 0001 2297 5165)