Location: Poultry Production and Product Safety Research
Project Number: 6022-32420-001-041-I
Project Type: Interagency Reimbursable Agreement
Start Date: Jul 1, 2021
End Date: Jun 30, 2024
Objective:
1. Determine the impact of heat stress at different stages of broiler chicken growth on neurochemical production within the intestinal and respiratory systems.
2. Determine the impact of heat stress at different stages of broiler chicken growth on the intestinal compositional and functional diversity of the microbiome using shotgun metagenomic sequencing.
3. Determine how E. coli responds to the simulated chicken intestinal environment, including exposure to neurochemicals, to understand how the bacteria cause respiratory infection in broiler chickens.
The long-term goal of this project is to utilize a novel mechanistic approach to generate high-quality research data into the underlying mechanisms by which heat stress in chicken broilers can lead to the emergence of Avian Pathogenic Escherichia coli (APEC). Infection of the chicken respiratory tract with APEC can result in the infectious disease known as colibacillosis which is a leading cause of mortality and economic loss to the poultry industry throughout the United States especially during the summer months. The performance of this research will lead to novel husbandry and therapeutic approaches to prevent colibacillosis due to APEC by providing the first-ever neurochemical biogeographical mapping of the broiler intestinal and respiratory systems in conjunction during heat stress conditions in conjunction with comprehensive microbiome analysis. This will provide a higher level of support to poultry producers throughout the United States, especially those who operate in areas which experience high levels of heat during the year.
Approach:
The grant application is based on the novel central hypothesis that heat stress in broilers produces a physiological response that results in the overproduction of stress-related neurochemicals within the gut and the lungs. It is specifically this production of stress neurochemicals that directly interacts with the microbiota within the gut, and Escherichia coli in particular, that provides the opportunity for the development of the APEC pathotype and the eventual development of colibacillosis. The host intestinal neurochemical stress responses thus alters the compositional and functional diversity of the microbiome resulting in a more permissive environment that, in turn, allows for stress neurochemicals to directly increase the growth and virulence production capabilities of E. coli. Further, this condition ‘primes’ the pathogenic potential of E. coli excreted in feces to contaminate the environment. Consequently, upon reaching the respiratory tract, and respiratory neurochemical stress response triggers infection by E. coli that originate from the gut. We will test this hypothesis in the following objectives:
Objective 1. Determine the impact of heat stress at different stages of broiler chicken growth on neurochemical production within the intestinal and respiratory systems.
Objective 2. Determine the impact of heat stress at different stages of broiler chicken growth on the intestinal compositional and functional diversity of the microbiome using shotgun metagenomic sequencing.
Objective 3. Determine how E. coli responds to the simulated chicken intestinal environment, including exposure to neurochemicals, to understand how the bacteria cause respiratory infection in broiler chickens.
We have employed this approach since the elucidation of the mechanisms that are at the root cause for the development of the APEC pathotype that is the cause of colibacillosis will have a long-term impact on the sustainability of the poultry industry in U.S. agriculture because by the completion of the project we anticipate that we will have: 1) identified functional, mechanistic pathways to understand how APEC infections occurs in broiler chickens, and 2) provided mechanistic explanations enabling the design of non-antibiotic-based approached for the treatment and prevention of APEC infection. The identification of the microbial mechanisms by which production-related heat stress contributes to E. coli infection in broiler chickens is expected to significantly improve our ability to prevent E. coli respiratory infection and colibacillosis.
