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The host/pathogen interaction is poorly understood because establishment of an
infection in livestock by a microorganism is a dynamic event. The complex interaction
between the host and the pathogen can now be explored in more detail using
microarrays.<P>
In this project, we will evaluate the genetic interaction of livestock
and pathogenic bacteria during colonization in an attempt to elucidate and interpret
the mechanistic roles of gene regulation in pathogenesis. Our goal is to develop a
comprehensive knowledge of host/pathogen interactions during colonization and to
elucidate how these interactions are affected by stress. These studies will lead to
new and/or improved diagnostic techniques, new therapeutics and vaccines, and
improved health management strategies for livestock.
Approach:<br/>
<p>Objective 1: Utilize microarray, microbiologic, and bioinformatic approaches in a ligated-intestinal model to elucidate host/pathogen genetic regulatory interactions during infection. Approach: We hypothesize that the pathogen, when introduced into the host environment, will regulate its virulence factors to adapt to the intestinal environment to achieve a colonized state. In turn, we expect the host will regulate its immune response at the site of infection to prevent or respond to the pathogen’s attempts to establish a foothold. We will utilize various molecular methods such as microarrays, in conjunction with a ligated intestinal model and directed colonization approach, to evaluate these interactions.</p>
<p>Objective 2: Using two stress models (transportation and neuroendocrine) in conjunction with Salmonella challenge in swine, develop an understanding of the relationship between various forms of stress and food borne pathogen susceptibility and shedding. Approach: Our hypothesis is that an animal has differential physiological and immunological responses to various stressors. These responses are unique to the type of stress encountered or experienced. Therefore, different stressors differentially affect a host’s susceptibility to, and shedding of, food borne pathogens. We will expose pigs to two types of stress. We hypothesis the initiation of a stress response via peripheral CRH should have a negative influence that will lower the natural immunity of the host and increase susceptibility to pathogens. If our hypothesis is correct, then a lower infectious dose of pathogen will be required to induce infection and shedding.</p>
<p>Objective 3: Model on-farm management practices to evaluate pathogen transmission in swine herds. Approach: The hypothesis is that there is a difference in pathogen transmission rates within swine herds which is dependent upon the type of housing system (group versus individual pens). This objective will be accomplished by experimentally infecting one individual within each type system and monitoring the spread of infection among the group. Individually, these separate transmission rates (pen or stall housing) can provide specific information on its particular system, but together these rates can be used in the future to design and generate more universal models and more appropriate rates for on-farm Salmonella herd transmission.</p>