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ARS Home » Plains Area » College Station, Texas » Southern Plains Agricultural Research Center » Food and Feed Safety Research » Research » Publications at this Location » Publication #392651

Research Project: Immunological and Practical Approaches to Manipulate the Ecological Niches and Reduce Foodborne Pathogens in Poultry

Location: Food and Feed Safety Research

Title: Chicken-specific kinome analysis of early host immune signaling pathways in the cecum of newly hatched chicks infected with Salmonella enterica serovar Enteriditis

item Kogut, Michael - Mike
item Genovese, Kenneth - Ken
item Byrd Ii, James - Allen
item Swaggerty, Christina - Christi
item He, Louis
item FARNELL, YUHUA - Texas A&M University
item ARSENAULT, RYAN - University Of Delaware

Submitted to: Frontiers in Cellular and Infection Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/30/2022
Publication Date: 6/30/2022
Citation: Kogut, M.H., Genovese, K.J., Byrd II, J.A., Swaggerty, C.L., He, L.H., Farnell, Y., Arsenault, R. 2022. Chicken-specific kinome analysis of early host immune signaling pathways in the cecum of newly hatched chicks infected with Salmonella enterica serovar Enteriditis. Frontiers in Cellular and Infection Microbiology. 12. Article 899395.

Interpretive Summary: Chicks get infected with Salmonella early in life, and it can survive in the chicks throughout their life. Because of this, the Salmonella can be consistently released from the birds and then infect other chicks. Also, the presence of Salmonella in the chicks when they go to market means that the Salmonella can get into chicken meat products potentially causing food poisoning in humans. The purpose of these experiments was to try to understand how Salmonella can survive in chicks for so long without being "seen" by the chick's immune system. We found that Salmonella causes a change in the immune response of the baby chicks so that they are "invisible" to the immune system. Thus, the immune cells cannot attack the Salmonella and kill it. These results are important to the pharmaceutical industry, because we have identified a specific target to stimulate the bird's immune system and provide protection against infection.

Technical Abstract: Poultry is a major source of human foodborne illness caused by broad host range Salmonella serovars (paratyphoid). 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 to 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. However, 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-a, and IFN-y; (3) Salmonella infection targeted the JAK-STAT pathway as a means of evading the host response by targeting the dephosphorylation of JAK1, 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 was activated through the AP-1 and NF-kB transcription factor cascades, but not through NFAT.