Chicken-Specific Kinome Array Reveals that Salmonella enterica Serovar Enteritidis Modulates Host Immune Signaling Pathways in the Cecum to Establish a Persistence Infection

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Author(s)Kogut, Michael H.
Author(s)Swaggerty, Christina L.
Author(s)Byrd, James Allen
Author(s)Selvaraj, Ramesh
Author(s)Arsenault, Ryan J.
Ordered AuthorMichael H. Kogut, Christina L. Swaggerty, James Allen Byrd, Ramesh Selvaraj and Ryan J. Arsenault
UD AuthorArsenault, Ryan Jen_US
Date Accessioned2016-10-12T14:12:02Z
Date Available2016-10-12T14:12:02Z
Copyright DateCopyright © 2016 by the authors; licensee MDPI, Basel, Switzerland.en_US
Publication Date2016-07-27
DescriptionPublisher's PDFen_US
AbstractNon-typhoidal Salmonella enterica induces an early, short-lived pro-inflammatory response in chickens that is asymptomatic of clinical disease and results in a persistent colonization of the gastrointestinal (GI) tract that transmits infections to naïve hosts via fecal shedding of bacteria. The underlying mechanisms that control this persistent colonization of the ceca of chickens by Salmonella are only beginning to be elucidated. We hypothesize that alteration of host signaling pathways mediate the induction of a tolerance response. Using chicken-specific kinomic immune peptide arrays and quantitative RT-PCR of infected cecal tissue, we have previously evaluated the development of disease tolerance in chickens infected with Salmonella enterica serovar Enteritidis (S. Enteritidis) in a persistent infection model (4–14 days post infection). Here, we have further outlined the induction of an tolerance defense strategy in the cecum of chickens infected with S. Enteritidis beginning around four days post-primary infection. The response is characterized by alterations in the activation of T cell signaling mediated by the dephosphorylation of phospholipase c-!1 (PLCG1) that inhibits NF-B signaling and activates nuclear factor of activated T-cells (NFAT) signaling and blockage of interferon-! (IFN-!) production through the disruption of the JAK-STAT signaling pathway (dephosphorylation of JAK2, JAK3, and STAT4). Further, we measured a significant down-regulation reduction in IFN-! mRNA expression. These studies, combined with our previous findings, describe global phenotypic changes in the avian cecum of Salmonella Enteritidis-infected chickens that decreases the host responsiveness resulting in the establishment of persistent colonization. The identified tissue protein kinases also represent potential targets for future antimicrobial compounds for decreasing Salmonella loads in the intestines of food animals before going to market.en_US
DepartmentUniversity of Delaware. Department of Animal and Food Sciences.en_US
CitationKogut, Michael H., et al. "Chicken-specific kinome array reveals that Salmonella enterica serovar Enteritidis modulates host immune signaling pathways in the cecum to establish a persistence infection." International Journal of Molecular Sciences 17.8 (2016): 1207.en_US
DOIdoi:10.3390/ijms17081207en_US
ISSN1661-6596 ; e- 1422-0067en_US
URLhttp://udspace.udel.edu/handle/19716/19799
Languageen_USen_US
PublisherMDPIen_US
dc.rightsThis article is an open access article distributed under the terms and conditions of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/).en_US
dc.sourceInternational Journal of Molecular Sciencesen_US
dc.source.urihttp://www.mdpi.com/journal/ijmsen_US
TitleChicken-Specific Kinome Array Reveals that Salmonella enterica Serovar Enteritidis Modulates Host Immune Signaling Pathways in the Cecum to Establish a Persistence Infectionen_US
TypeArticleen_US
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