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Transcriptional responses in spleens from mice exposed to Yersinia pestis CO92
James V Rogers1, Young W Choi, Lenore F Giannunzio
1Battelle Memorial Institute, 505 King Avenue, JM-7, Columbus, OH 43201, USA. rogersjv@battelle.org
Abstract:
Yersinia pestis is one of the most threatening biological agents due to the associated high mortality and history of plague pandemics. Identifying molecular players in the host response to infection may enable the development of medical countermeasures against Y. pestis. In this study, microarrays were used to identify the host splenic response mechanisms to Y. pestis infection. Groups of Balb/c mice were injected intraperitoneally with 2-257CFU of Y. pestis strain CO92 or vehicle. One group was assessed for mortality rates and another group for transcriptional analysis. The time to death at the 8 and 257CFU challenge doses were 5.0+/-2.3 and 3.8+/-0.4 days, respectively. Gene profiling using Affymetrix Mouse Genome 430 2.0 Arrays revealed no probe sets were significantly altered for all five mice in the low-dose group when compared to the vehicle controls. However, 534 probe sets were significantly altered in the high dose versus vehicle controls; 384 probe sets were down-regulated and 150 probe sets were up-regulated. The predominant biological processes identified were immune function, cytoskeletal, apoptosis, cell cycle, and protein degradation. This study provides new information on the underlying transcriptional mechanisms in mice to Y. pestis infection.
Insights
Yersinia pestis infection in mice revealed significant splenic gene expression changes, particularly at high doses. This study identifies key host response mechanisms to plague, aiding in developing countermeasures.
Area of Science:
- Microbiology
- Immunology
- Genomics
Background:
- Yersinia pestis causes plague, a historically devastating disease with high mortality.
- Understanding host responses is crucial for developing effective medical countermeasures.
- The spleen plays a key role in the immune response to bacterial infections.
Purpose of the Study:
- To identify host splenic transcriptional mechanisms during Yersinia pestis infection.
- To investigate the dose-dependent host response to Y. pestis.
- To provide insights into molecular players involved in Y. pestis pathogenesis.
Main Methods:
- Balb/c mice were infected intraperitoneally with Yersinia pestis strain CO92 at low (2 CFU) and high (257 CFU) doses.
- Mortality rates and time to death were recorded.
- Transcriptional analysis was performed using Affymetrix Mouse Genome 430 2.0 Arrays.
Main Results:
- No significant transcriptional alterations were observed in the low-dose Y. pestis infection group.
- In the high-dose group, 534 probe sets were significantly altered, with 384 down-regulated and 150 up-regulated.
- Predominant affected biological processes included immune function, cytoskeletal organization, apoptosis, cell cycle, and protein degradation.
Conclusions:
- High-dose Yersinia pestis infection induces significant transcriptional changes in the mouse spleen.
- The identified transcriptional alterations highlight key host response pathways, including immune and cellular processes.
- This study offers valuable data for understanding the host-pathogen interactions during plague infection.
