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EVALUATING VIRULENCE OF WATERBORNE AND CLINCIAL AEROMONAS ISOLATES USING GENE EXPRESSION AND MORTALITY IN NEONATAL MICE FOLLOWED BY ASSESSING CELL CULTURE'S ABILITY TO PREDICT VIRULENCE BASED ON TRANSCRIPTIONAL RESPONSE
Citation:
HAYES, S. L., M. R. RODGERS, D. J. LYE, G. N. STELMA, C. A. MCKINSTRY, J. M. MALARD, AND S. J. VESPER. EVALUATING VIRULENCE OF WATERBORNE AND CLINCIAL AEROMONAS ISOLATES USING GENE EXPRESSION AND MORTALITY IN NEONATAL MICE FOLLOWED BY ASSESSING CELL CULTURE'S ABILITY TO PREDICT VIRULENCE BASED ON TRANSCRIPTIONAL RESPONSE. A. Gilmour (ed.), JOURNAL OF APPLIED MICROBIOLOGY. Blackwell Publishing, Malden, MA, 103(4):811-820, (2007).
Impact/Purpose:
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Description:
The virulence of multiple Aeromonas spp. were assessed using two models, a neonatal mouse assay and a mouse intestinal cell culture. Transcriptional responses to both infection models were assessed using microarrays. After artificial infection with a variety of Aeromonas spp., mRNA extracts from the two models were processed and hydridized to murine microarrays to determine host gene response. Definition of virulence was determined based on host mRNA production in murine neonatal intestinal tissue and morbidity or mortality of infected animals. Infections of mouse intestinal cell cultures were then performed to determine whether this simpler model system's mRNA responses correlated to neonatal results and therefore be predictive of virulence of Aeromonas spp. Virulent aeromonads up-regulated transcripts in both models including multiple host defense gene products (chemokines, regulation of transcription and apoptosis, cell signaling). Avirulent species exhibited little or no host response in neonates. Morbidity and mortality results correlated well with both bacterial dose and host gene expression in the neonatal mice. Cell culture results were less discriminating but showed promise as potentially being able to be predictive of virulence. Jun oncogene up-regulation in murine cell culture is potentially predictive of Aeromonas virulence.