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The bacterial exotoxin AIP56 induces fish macrophage and neutrophil apoptosis using mechanisms of the extrinsic and intrinsic pathways
Authors:Carolina Costa-Ramos  Ana do Vale  Paula Ludovico  Nuno MS dos Santos  Manuel T Silva
Institution:1. Fish Immunology and Vaccinology Group, IBMC – Instituto de Biologia Molecular e Celular, Universidade do Porto, Rua do Campo Alegre, 823, 4150-180 Porto, Portugal;2. Life and Health Sciences Research Institute (ICVS), School of Health Sciences, University of Minho, Campus de Gualtar, Braga 4710-057, Portugal;1. Laboratory of Biochemistry and Molecular Biology, School of Marine Sciences, Meishan Campus, Ningbo University, Ningbo, 315800, China;2. Key Laboratory of Applied Marine Biotechnology of Ministry of Education, Meishan Campus, Ningbo University, Ningbo, 315800, China;1. Department of Aquatic Animal Medicines, College of Fisheries, Huazhong Agricultural University, Wuhan, Hubei 430070, China;2. Hubei Engineering Technology Research Center for Aquatic Animal Diseases Control and Prevention, China;3. Bio-Transduction Lab, Wuhan Institute of Biotechnology, Wuhan 430075, China;1. Department of Animal Science, Faculty of Animal Science and Food Technology, Agricultural Sciences and Natural Resources University of Khuzestan, P.O. Box 63417, 73637, Mollasani, Ahvaz, Iran;2. Department of Animal Science, College of Agriculture, Isfahan University of Technology, Isfahan 84156-83111, Iran
Abstract:It has been previously shown that the exotoxin of the important fish pathogen Photobacterium damselae ssp. piscicida is a key pathogenicity factor and is responsible for the extensive systemic apoptosis of macrophages and neutrophils seen in acute fish photobacteriosis. The focus of the present study was to further characterize the AIP56-induced apoptosis of sea bass professional phagocytes by assessing the involvement of caspases, mitochondria and oxidative stress. The resulting data indicate that the apoptotic response in peritoneal macrophages and neutrophils treated ex vivo with AIP56 involves activation of caspase-8, -9 and -3, and mitochondria as shown by loss of mitochondrial membrane potential, release of cytochrome c and over-production of ROS. These results together with previous data from this laboratory suggest that both the extrinsic and intrinsic apoptotic pathways are involved in the AIP56-induced phagocyte apoptosis.
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