Rise Matthew L, Jones Simon R M, Brown Gordon D, von Schalburg Kristian R, Davidson William S, Koop Ben F
Great Lakes Wisconsin Aquatic Technology and Environmental Research (WATER) Institute, University of Wisconsin-Milwaukee,
Physiol Genomics. 2004 Dec 15;20(1):21-35. doi: 10.1152/physiolgenomics.00036.2004. Epub 2004 Sep 28.
Piscirickettsia salmonis is the intracellular bacterium that causes salmonid rickettsial septicemia, an infectious disease that kills millions of farmed fish each year. The mechanisms used by P. salmonis to survive and replicate within host cells are not known. Piscirickettsiosis causes severe necrosis of hematopoietic kidney. Microarray-based experiments with QPCR validation were used to identify Atlantic salmon macrophage and hematopoietic kidney genes differentially transcribed in response to P. salmonis infection. Infections were confirmed by microscopy and RT-PCR with pathogen-specific primers. In infected salmon macrophages, 71 different transcripts were upregulated and 31 different transcripts were downregulated. In infected hematopoietic kidney, 30 different transcripts were upregulated and 39 different transcripts were downregulated. Ten antioxidant genes, including glutathione S-transferase, glutathione reductase, glutathione peroxidase, and cytochrome b558 alpha- and beta-subunits, were upregulated in infected macrophages but not in infected hematopoietic kidney. Changes in redox status of infected macrophages may allow these cells to tolerate P. salmonis infection, raising the possibility that treatment with antioxidants may reduce hematopoietic tissue damage caused by this rickettsial infection. The downregulation of transcripts involved in adaptive immune responses (e.g., T cell receptor alpha-chain and C-C chemokine receptor 7) in infected hematopoietic kidney but not in infected macrophages may contribute to infection-induced kidney tissue damage. Molecular biomarkers of P. salmonis infection, characterized by immune-relevant functional annotations and high fold differences in expression between infected and noninfected samples, may aid in the development of anti-piscirickettsial vaccines and therapeutics.
鲑鱼立克次氏体是一种细胞内细菌，可引发鲑科立克次氏体败血症，这是一种每年导致数百万养殖鱼类死亡的传染病。鲑鱼立克次氏体在宿主细胞内存活和复制所采用的机制尚不清楚。鲑鱼立克次氏体病会导致造血肾严重坏死。基于微阵列并经定量聚合酶链反应验证的实验，用于鉴定大西洋鲑巨噬细胞和造血肾中因感染鲑鱼立克次氏体而差异转录的基因。通过显微镜检查以及使用病原体特异性引物进行逆转录聚合酶链反应来确认感染情况。在受感染的鲑鱼巨噬细胞中，71种不同的转录本上调，31种不同的转录本下调。在受感染的造血肾中，30种不同的转录本上调，39种不同的转录本下调。包括谷胱甘肽S - 转移酶、谷胱甘肽还原酶、谷胱甘肽过氧化物酶以及细胞色素b558的α和β亚基在内的10种抗氧化基因，在受感染的巨噬细胞中上调，但在受感染的造血肾中未上调。受感染巨噬细胞氧化还原状态的变化可能使这些细胞耐受鲑鱼立克次氏体感染，这增加了用抗氧化剂治疗可能减少这种立克次氏体感染引起的造血组织损伤的可能性。在受感染的造血肾而非受感染的巨噬细胞中，参与适应性免疫反应的转录本（如T细胞受体α链和C - C趋化因子受体7）下调，这可能导致感染引起的肾组织损伤。以免疫相关功能注释以及感染样本与未感染样本之间高倍数表达差异为特征的鲑鱼立克次氏体感染分子生物标志物，可能有助于抗鲑鱼立克次氏体疫苗和治疗方法的开发。
