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J Med Microbiol 55 (2006), 263-271; DOI: 10.1099/jmm.0.46313-0
© 2006 Society for General Microbiology
ISSN 0022-2615

Transcriptional profiling of host responses in mouse lungs following aerosol infection with type A Francisella tularensis

Henrik Andersson1, Blanka Hartmanová1,3, Rhonda KuoLee2, Patrik Rydén1, Wayne Conlan2, Wangxue Chen2 and Anders Sjöstedt1

1 Department of Clinical Microbiology, Clinical Bacteriology, Umeå University, SE-901 85 Umeå, Sweden

2 National Research Council Canada, Institute for Biological Sciences, Ottawa, Ontario, K1A 0R6, Canada

3 Proteome Center for the Study of Intracellular Parasitism of Bacteria, Faculty of Military Health Science, University of Defence, Trebesská 1575, 500 01 Hradec Králové, Czech Republic

Correspondence
Anders Sjöstedt
Anders.Sjostedt{at}climi.umu.se

Received 1 September 2005
Accepted 28 October 2005

Tularaemia caused by inhalation of type A Francisella tularensis bacteria is one of the most aggressive infectious diseases known, but the reasons for the very rapid spread of the organism from the lungs to internal organs and the ensuing mortality are unknown. The present study used the mouse model to examine in detail the host immune response in the lung. After an aerosol challenge with 20 c.f.u. of the type A strain FSC033, all mice developed clinical signs of severe disease, showed weight loss by day 4 of infection and died the next day. Histopathological findings in the lung revealed acute inflammation and intense vasculitis and perivasculitis on day 4. Gene transcriptional changes in the mouse lung samples were examined on days 1, 2 and 4 of infection using a cDNA microarray with 20 600 mouse clones representing 18 500 genes. In total, 424 genes were found to be differentially expressed, some of which were both up- and downregulated at different time points, 192 of which were upregulated and 234 of which were downregulated for at least one time point. A high percentage of selected genes identified by the microarray analysis were confirmed to be differentially regulated by quantitative real-time PCR. Categorization of the differentially expressed genes showed that those preferentially involved in host immune responses were activated extensively on day 4 but hardly or not at all on days 1 and 2. Further analysis revealed that several of the genes upregulated on day 4 are known to depend on gamma interferon or tumour necrosis factor alpha for their regulation. In keeping with this finding, tumour necrosis factor alpha and gamma interferon levels were found to be increased significantly in bronchoalveolar lavage on day 4.




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