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ARS Home » Midwest Area » Ames, Iowa » National Animal Disease Center » Food Safety and Enteric Pathogens Research » Research » Publications at this Location » Publication #191971
Title: TRANSCIPTIONAL SUPPRESSION OF SPECIFIC PORCINE IMMUNE PATHWAYS DURING INFECTION WITH SALMONELLA ENTERICA SEROTYPE TYPHIMURIUM COMPARED TO CHOLERAESUIS

Author
item WANG, Y - IOWA STATE UNIVERSITY
item UTHE, J - IOWA STATE UNIVERSITY
item Bearson, Shawn
item Kuhar, Daniel
item Lunney, Joan
item QU, L - IOWA STATE UNIVERSITY
item COUTURE, O - IOWA STATE UNIVERSITY
item NETTLETON, D - IOWA STATE UNIVERSITY
item TUGGLE, C - IOWA STATE UNIVERSITY

Submitted to: International Plant and Animal Genome IX Conference
Publication Type: Abstract Only
Publication Acceptance Date: 11/4/2005
Publication Date: 1/14/2006
Citation: Wang, Y.F., Uthe, J.J., Bearson, S.M., Kuhar, D.J., Lunney, J.K., Qu, L., Couture, O., Nettleton, D., Tuggle, C.K. 2006. Transciptional suppression of specific porcine immune pathways during infection with Salmonella enterica serotype Typhimurium compared to Choleraesuis [abstract]. International Plant and Animal Genome IX Conference. p. W242.

Interpretive Summary:

Technical Abstract: Salmonellosis is prevalent worldwide and is both a food safety issue and production problem. Classic salmonellae of pigs are S. enterica serotype Choleraesuis (SC) and Typhimurium (ST). To understand the host transcriptional response to infection, total RNA was collected from the mesenteric lymph nodes of uninfected pigs or pigs inoculated with each serotype at 8 hours (H), 24H, 48H and 21 days (D) post-inoculation (PI) (n=30 pigs). An ANOVA analysis of data collected using the Affymetrix GeneChip® found the following numbers of differentially expressed genes (P < 0.01, Fold change > 2, q < 0.26) during ST infection: 8H, 173 genes; 24H, 224 genes; 48H, 179 genes. For the SC infection, data analysis showed: 8H, 150 genes; 24H, 251 genes; 48H, 1175 genes. Quantitative RT-PCR analysis verified the expression patterns of 12 of 13 innate immunity genes. To understand how ST may escape the host immune system, we studied genes differentially expressed in response to ST but unaffected (p>0.05) during SC infection. Genes involved in the NFkB pathway (MTPN, PTPN13 and PTPN6) or apoptosis (CIDEB, CASP4) were down-regulated early in infection, while some potential inhibitory genes (GNAI1, GYS1, MAP3K11 and TBX2) were up-regulated. These data indicate that ST may suppress specific innate immune pathways and thereby elude the strong inflammatory response observed during SC infection. We are currently validating these expression patterns, as well as integrating data from the Qiagen 13K platform collected from SC infected lung tissue RNA, to gain a more global understanding of host response to infection.