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The specific transcriptomic response of porcine intestinal epithelial cells to Escherichia coli and Salmonella enterica Typhimurium infections is modulated by bovine colostrum fractions
Journal article   Open access   Peer reviewed

The specific transcriptomic response of porcine intestinal epithelial cells to Escherichia coli and Salmonella enterica Typhimurium infections is modulated by bovine colostrum fractions

Mylene Blais, Michael Bouchard, Ckaude Asselin and Martin Lessard
The Journal of immunology (1950), v 204(1_Supplement), pp 79-79.9
01 May 2020
DOI: https://doi.org/10.4049/jimmunol.204.Supp.79.9
url
https://doi.org/10.1002/batt.202200432View
Published, Version of Record (VoR)CC BY V4.0,  Open

Abstract

Abstract Enterotoxigenic Escherichiacoli (ETEC) and Salmonella enterica Typhimurium are both enteric pathogens, but the mechanisms by which they infect intestinal epithelium are different. Recently, we observed that bovine colostrum (BC) increases protection against enteric infections in weaned piglets. In this study, we described the transcriptomic response of porcine intestinal epithelial cells IPEC-J2 infected by each pathogens, and we measured the specific effect of defatted BC, as well as bovine serocolostrum and casein fractions (SC and CAS respectively) on IPEC-J2 transcriptomic response to ETEC and Salmonella by microarray analysis. We also measured the impact of BC, SC and CAS on pathogen-induced epithelial integrity loss using transepithelial electrical resistance (TEER), and on NF-kB transcriptional activity by luciferase assays. Results showed that transcriptomic profile of cells challenged with ETEC and Salmonella both induced genes involved in inflammatory response, while ETEC specifically induced the expression of genes involved in morphogenesis and response to lipids, and Salmonella specifically regulated genes involved in oxidative stress, migration and apoptotic process. The ETEC induction of inflammatory genes was decreased by BC and SC, while Salmonella induction of inflammatory genes was specifically reduced by BC and CAS fraction. BC prevented epithelial integrity disruption caused by both pathogens, while SC only prevented the one caused by Salmonella. Finally, BC and SC decreased NF-kB activity induced by each pathogen. Altogether, these results indicated that BC fractions modulate in a specific manner cellular mechanisms involved in intestinal epithelial response to these pathogens.

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