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Physiol. Genomics (September 28, 2004). doi:10.1152/physiolgenomics.00036.2004 Free Article
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Submitted on February 11, 2004
Accepted on September 24, 2004

Microarray analyses identify molecular biomarkers of Atlantic salmon macrophage and hematopoietic kidney response to Piscirickettsia salmonis infection

Matthew L Rise1, Simon R. M Jones2, Gordon D Brown3, Kristian R von Schalburg3, William S Davidson4, and Ben F Koop3*

1 Great Lakes WATER Institute, University of Wisconsin-Milwaukee, Milwaukee, WI, USA
2 Pacific Biological Station, Fisheries and Oceans Canada, Nanaimo, BC, Canada
3 Centre for Biomedical Research, University of Victoria, Victoria, BC, Canada
4 Molecular Biology and Biochemistry, Simon Fraser University, Burnaby, BC, Canada

* To whom correspondence should be addressed. E-mail: bkoop{at}uvic.ca.

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 RTPCR with pathogen-specific primers. In infected salmon macrophages, 71 different transcripts were up-regulated and 31 different transcripts were down-regulated. In infected hematopoietic kidney, 30 different transcripts were up-regulated and 39 different transcripts were down-regulated. Ten antioxidant genes, including glutathione S-transferase, glutathione reductase, glutathione peroxidase, and cytochrome b558 alpha and beta subunits, were up-regulated 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 down-regulation 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 non-infected samples, may aid in the development of anti-piscirickettsial vaccines and therapeutics.




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