The 94th Annual Meeting of Japanese Society for Bacteriology

Presentation information

On-demand Presentation

6 Virulence Factors and Biophylaxis

[ODP6B] b. Toxins, Effectors, and Bioactive Substances

[ODP-128] SubAB induces a novel form of Lipocalin 2, which involves in STEC survival

○Kinnosuke Yahiro1, Kohei Ogura2, Yoshiyuki Goto3, Sunao Iyoda4, Makoto Ohnishi4 (1Dept. Molecular Infectiology, Grad. Sch. Medicine, Chiba Univ., 2Advanced Health Care Science Research Unit, Institute for Frontier Science Initiative, Kanazawa Univ., 3Div. Molecular Immunology, Medical Mycology Research Center, Chiba Univ., 4Dept. Bacteriology I, National Institute of Infectious Diseases)

Shiga-toxigenic Escherichia coli (STEC) infection causes severe bloody diarrhea, renal failure, and hemolytic uremic syndrome (HUS). 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. Here, we demonstrates 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 PERK via CHOP 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.