Yersinia pseudotuberculosis Exploits CD209 Receptors for Promoting Host Dissemination and Infection
INFECTION AND IMMUNITY
Authors: He, Ying-Xia; Ye, Cheng-Lin; Zhang, Pei; Li, Qiao; Park, Chae Gyu; Yang, Kun; Jiang, Ling-Yu; Lv, Yin; Ying, Xiao-Ling; Ding, Hong-Hui; Huang, Hong-Ping; Tembo, John Mambwe; Li, An-Yi; Cheng, Bing; Zhang, Shu-Sheng; Zheng, Guo-Xing; Chen, Shi-Yun; Li, Wei; Xia, Lian-Xu; Kan, Biao; Wang, Xin; Jing, Huai-Qi; Yang, Rui-Fu; Peng, Hua; Fu, Yang-Xin; Klena, John D.; Skurnik, Mikael; Chen, Tie
Abstract
Yersinia pseudotuberculosis is a Gram-negative enteropathogen and causes gastrointestinal infections. It disseminates from gut to mesenteric lymph nodes (MLNs), spleen, and liver of infected humans and animals. Although the molecular mechanisms for dissemination and infection are unclear, many Gram-negative enteropathogens presumably invade the small intestine via Peyer's patches to initiate dissemination. In this study, we demonstrate that Y. pseudotuberculosis utilizes its lipopolysaccharide (LPS) core to interact with CD209 receptors, leading to invasion of human dendritic cells (DCs) and murine macrophages. These Y. pseudotuberculosis CD209 interactions result in bacterial dissemination to MLNs, spleens, and livers of both wild-type and Peyer's patch-deficient mice. The blocking of the Y. pseudotuberculosis CD209 interactions by expression of 0-antigen and with oligosaccharides reduces infectivity. Based on the well-documented studies in which HIV-CD209 interaction leads to viral dissemination, we therefore propose an infection route for Y. pseudotuberculosis where this pathogen, after penetrating the intestinal mucosal membrane, hijacks the Y. pseudotuberculosis CD209 interaction antigen-presenting cells to reach their target destinations, MLNs, spleens, and livers.
Immune gene expression in trout cell lines infected with the fish pathogenic oomycete Saprolegnia parasitica
DEVELOPMENTAL AND COMPARATIVE IMMUNOLOGY
Authors: de Bruijn, Irene; Belmonte, Rodrigo; Anderson, Vicky L.; Saraiva, Marcia; Wang, Tiehui; van West, Pieter; Secombes, Christopher J.
Abstract
The oomycete Saprolegnia parasitica causes significant losses in the aquaculture industry, mainly affecting salmon, trout and catfish. Since the ban of malachite green, effective control measures are currently not available prompting a re-evaluation of the potential for immunological intervention. In this study, the immune response of salmonid cells is investigated at the transcript level, by analysis of a large set of immune response genes in four different rainbow trout cell lines (RTG-2, RTGill, RTL and RTS11) upon infection with S. parasitica. Proinflammatory cytokine transcripts were induced in all four cell lines, including IL-1 beta 1, IL-8, IL-11, INF-alpha 2, as well as other components of the innate defences, including COX-2, the acute phase protein serum amyloid A and C-type lectin CD209a and CD209b. However, differences between the four cell lines were found. For example, the fold change of induction was much higher in the epithelial RTL and macrophage-like RTS11 cell lines compared to the fibroblast cell lines RTG-2 and RTGill. Several antimicrobial peptides (AMPs) were also up-regulated in response to Saprolegnia infection, including hepcidin and cathelicidin 1 (rtCATH1) and 2 (rtCATH2). An rtCATH2 peptide was synthesised and tested for activity and whilst it showed no killing activity for zoospores, it was able to delay sporulation of S. parasitica. These results demonstrate that particular immune genes are up-regulated in response to S. parasitica infection and that AMPs may play a crucial role in the first line of defence against oomycetes in fish. (C) 2012 Elsevier Ltd. All rights reserved.