Lymphoid apoptosis in Edwardsiella tarda septicemia in tilapia, Oreochromis niloticus Nopadon Pirarat a,b , Masashi Maita b , Makoto Endo b , Takayuki Katagiri b, * a Department of Pathology, Faculty of Veterinary Science, Chulalongkorn University, Bangkok 10330, Thailand b Laboratory of Fish Health Management, Tokyo University of Marine Science and Technology, 4-5-7 Konan, Minato, Tokyo 108-8477, Japan Received 3 June 2006; revised 14 July 2006; accepted 3 August 2006 Available online 17 August 2006 Abstract The present study revealed a relationship between the kinetic change of apoptosis and the inflammatory response during exper- imental intraperitoneal infection with Edwardsiella tarda as a septicemic model. The morphological changes of apoptotic cells including cellular shrinkage, condensed nuclear chromatin, nuclear fragmentation and membrane blebbing were detected by light and transmission electron microscopy. TUNEL and agarose gel electrophoresis confirmed the fragmentation of DNA in the apo- ptotic cells. Apoptosis was highly detected in lymphoid organs prior to the inflammatory process and gradually decreased after an extensive inflammatory response. Apoptosis in thymus and spleen was extensive and an in vitro study revealed that lymphocytes were the major cell population which underwent apoptosis. The result suggests that E. tarda-induced systemic immunosuppression via lymphocyte apoptosis as determined by suppression of the systemic inflammatory response during an initial step of generalized septicemia. Ó 2006 Elsevier Ltd. All rights reserved. Keywords: Edwardsiella tarda; Oreochromis niloticus; Septicemia; Apoptosis 1. Introduction Since its discovery in the late 1960s, Edwardsiella tarda, a virulent intracellular bacterium capable of infecting var- ious types of cells, has been recognized as an important pathogen of commercial fish species such as eel, flounder, chan- nel catfish, carp, tilapia and others [1]. The major characteristics of edwardsiellosis include systemic inflammatory response, generalized septicemia and eventual death. Under natural conditions, primary septicemia is mainly caused by waterborne contact especially through septic wound. The mortality rate can be as high as 80% [2]. To understand the mechanism of the disease, a variety of responses in the host-pathogen interaction including phagocytosis of the pathogen, release of cytokines, secretion of toxins, as well as production of reactive oxygen species (ROS) have been increasingly revealed [3e5]. * Corresponding author. Tel./fax: þ81 3 5463 0546. E-mail address: takakata@s.kaiyodai.ac.jp (T. Katagiri). 1050-4648/$ - see front matter Ó 2006 Elsevier Ltd. All rights reserved. doi:10.1016/j.fsi.2006.08.007 Fish & Shellfish Immunology 22 (2007) 608e616 www.elsevier.com/locate/fsi