Location: Poultry Production and Product Safety Research
Project Number: 6022-32420-001-022-S
Project Type: Non-Assistance Cooperative Agreement
Start Date: Sep 1, 2022
End Date: Dec 31, 2025
Objective:
1. Identify the role that environmental stress-induced enteric dysfunction causes local neuroimmune responses that could affect Electron (E)-beam vaccine efficacy in poultry. Stress-related neurochemicals, such as serotonin, are intimately linked to immune function in the gut, including T-cell responses that are essential for vaccine efficacy. Understanding how physiological stressors in the pre-harvest stage alter the poultry gut neuroimmune environment will provide essential information for the successful delivery and application of novel antibiotic-alternative vaccines, including E-beam-killed vaccines.
2. Examine how the food composition of the poultry diet is a critical factor in providing neurochemical-based substrates impact the gut neuroimmune environment to determine the ability of gut foodborne pathogens growth and colonization. The poultry diet has been shown to contain plant-based neurochemicals that are exactly the same as that produced within the poultry gut, including those that affect inflammation and immune profile—elements that are essential in electron (E)-beam vaccine efficacy. Understanding how the poultry diet can contribute plant-based neurochemicals that can influence neuroimmune elements of the gut will provide another novel non-antibiotic platform by which to control the colonization of foodborne pathogens in the poultry gut.
Approach:
The need for the development of antibiotic alternatives to reduce foodborne pathogens in poultry production is a major focus of research at the USDA-ARS and the University of Arkansas and an area in which the combined efforts of each can synergize the overall research. Of particular interest is the reduction in the burden of the enteric pathogens Salmonella and Campylobacter, as they are two of the most prevalent foodborne pathogens that colonize poultry and cause significant illness when consumed by the general public. Work that has been performed in a large range of other animal species including humans has shown that bacterial pathogens can recognize stress-related neurochemicals and immediately change their physiology to survive in the gut. One critical aspect of the neurochemical-induced change in physiology are alterations in the gut neuroimmune environment that influence pathogen ability to colonize thereby further contaminating the bird and presenting a major challenge to the poultry industry to provide a safe product to the consumer. As vaccines are used in the poultry industry, and the efficacy of vaccines relies on the poultry immune system, understanding how stress-based neurochemical changes can alter the neuroimmune environment in the gut is essential to optimizing efficacy of novel vaccine technologies, such as electron (E)-beam, that seek to reduce Campylobacter or Salmonella foodborne pathogens in the poultry gut.
While the ability of stress neurochemicals to affect neuroimmune parameters important in vaccine control of gut pathogens has been amply shown in non-avian related species, much less is known in the specifics of how it functions in poultry. Hence, we will investigate how neurochemicals released in the chicken gut during periods of stress can influence the neuroimmune physiology of the poultry gut, and affect vaccine efficacy, to mediate colonization by foodborne pathogens Campylobacter and Salmonella. To achieve our goal we will use a range of cutting-edge analytical techniques including ultra-high-performance liquid chromatography to quantitatively assess neurochemical changes in the gut as a consequence of stress, 2-D protein gel electrophoresis to detect protein surface changes in Salmonella and Campylobacter that have been exposed to stress neurochemicals in concentrations found in the gut, tandem mass spectrometry to determine relevant proteomic changes, and Ussing chamber to assess how neurochemical physiologically induced Salmonella and Campylobacter change their ability to invade gut tissues. We will also apply these same techniques to the quantification of neurochemical substrates in chicken feed and examine how these substrates are utilized by Salmonella and Campylobacter. It is anticipated that the mechanisms governing the ability for neurochemicals and neurochemical substrates will be identified that will inform the design of novel non-antibiotic mediated means by which to interrupt the ability of foodborne pathogens to recognize and subsequently utilize neurochemicals and substrates to colonize the poultry gut and present a food safety issue, thereby providing significant value to the industry.
