Dataset Information

Differential Levels of Cecal Colonization by Salmonella Enteritidis in Chickens Triggers Distinct Immune Kinome Profiles.

ABSTRACT: Salmonella enterica serovar Enteritidis are facultative intracellular bacteria that cause disease in numerous species. Salmonella-related infections originating from poultry and/or poultry products are a major cause of human foodborne illness with S. Enteritidis the leading cause worldwide. Despite the importance of Salmonella to human health and chickens being a reservoir, little is known of the response to infection within the chicken gastrointestinal tract. Using chicken-specific kinome immune peptide arrays we compared a detailed kinomic analysis of the chicken jejunal immune response in a single line of birds with high and low Salmonella loads. Four-day-old chicks were challenged with S. Enteritidis (105?cfu) and cecal content and a section of jejunum collected at three times: early [4-7?days post-infection (dpi)], middle (10-17?dpi), and late (24-37?dpi). Salmonella colonization was enumerated and birds with the highest (n?=?4) and lowest (n?=?4) loads at each time were selected for kinomic analyses. Key biological processes associated with lower loads of Salmonella clustered around immune responses, including cell surface receptor signaling pathway, positive regulation of cellular processes, defense response, innate immune response, regulation of immune response, immune system process, and regulation of signaling. Further evaluation showed specific pathways including chemokine, Jak-Stat, mitogen activated protein kinase, and T cell receptor signaling pathways were also associated with increased resistance. Collectively, these findings demonstrate that it is possible to identify key mechanisms and pathways that are associated with increased resistance against S. Enteritidis cecal colonization in chickens. Therefore, providing a foundation for future studies to identify specific proteins within these pathways that are associated with resistance, which could provide breeders additional biomarkers to identify birds naturally more resistant to this important foodborne pathogen.

SUBMITTER: Swaggerty CL

PROVIDER: S-EPMC5733560 | biostudies-literature | 2017

REPOSITORIES: biostudies-literature

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Differential Levels of Cecal Colonization by Salmonella Enteritidis in Chickens Triggers Distinct Immune Kinome Profiles.

Swaggerty Christina L CL Kogut Michael H MH He Haiqi H Genovese Kenneth J KJ Johnson Casey C Arsenault Ryan J RJ

Frontiers in veterinary science 20171213

Salmonella enterica serovar Enteritidis are facultative intracellular bacteria that cause disease in numerous species. Salmonella-related infections originating from poultry and/or poultry products are a major cause of human foodborne illness with S. Enteritidis the leading cause worldwide. Despite the importance of Salmonella to human health and chickens being a reservoir, little is known of the response to infection within the chicken gastrointestinal tract. Using c ...[more]

PMID: 29322049

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Project description:Poultry is a major source of human foodborne illness caused by broad host range Salmonella serovars (paratyphoid), and developing cost-effective, pre-harvest interventions to reduce these pathogens would be valuable to the industry and consumer. Host responses to infectious agents are often regulated through phosphorylation. However, proteomic mechanisms of Salmonella acute infection biology and host responses to the bacteria have been limited concentrating predominately on the genomic responses of the host to infection. Our recent development of chicken-specific peptide arrays for kinome analysis of host phosphorylation-based cellular signaling responses provided us with the opportunity to develop a more detailed understanding of the early (4-24 h post-infection) host-pathogen interactions during the initial colonization of the cecum by Salmonella. Using the chicken-specific kinomic immune peptide array, biological pathway analysis showed infection with S. Enteritidis increased signaling related to the innate immune response, relative to the non-infected control ceca. Notably, the acute innate immune signaling pathways were characterized by increased peptide phosphorylation (activation) of the Toll-like receptor and NOD-like receptor signaling pathways, the activation of the chemokine signaling pathway, and the activation of the apoptosis signaling pathways. In addition, Salmonella infection induced a dramatic alteration in the phosphorylation events of the JAK-STAT signaling pathway. Lastly, there is also significant activation of the T cell receptor signaling pathway demonstrating the initiation of the acquired immune response to Salmonella infection. Based on the individual phosphorylation events altered by the early Salmonella infection of the cecum, certain conclusions can be drawn: (1) Salmonella was recognized by both TLR and NOD receptors that initiated the innate immune response; (2) activation of the PPRs induced the production of chemokines CXCLi2 (IL-8) and cytokines IL-2, IL-6, IFN-α, and IFN-γ; (3) Salmonella infection targeted the JAK-STAT pathway as a means of evading the host response by targeting the dephosphorylation of JAK1 and TYK2 and STAT1,2,3,4, and 6; (4) apoptosis appears to be a host defense mechanism where the infection with Salmonella induced both the intrinsic and extrinsic apoptotic pathways; and (5) the T cell receptor signaling pathway activates the AP-1 and NF-κB transcription factor cascades, but not NFAT.

Dataset Information

Differential Levels of Cecal Colonization by Salmonella Enteritidis in Chickens Triggers Distinct Immune Kinome Profiles.

Publications

Differential Levels of Cecal Colonization by <i>Salmonella</i> Enteritidis in Chickens Triggers Distinct Immune Kinome Profiles.

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