|PARK, SOON - BARC VIST. SY
|PARK, DOON - BARC VIST. SY
|FITZCOY, STEVE - SCHERING-PLOUGH
|BAUTISTA, DANIEL - UNIV. DELAWARE
Submitted to: Meeting Proceedings
Publication Type: Proceedings
Publication Acceptance Date: 1/1/2007
Publication Date: 7/14/2007
Citation: Lillehoj, H.S., Park, S.S., Allen, P., Park, D.W., Fitzcoy, S., Bautista, D.A. 2007. Innate immune response to Clostridium perfringens and Eimeria maxima in necrotic enteritis model.Proceedings of America Avian veterinary pathologists, July 14-18, Washington, D.C.
Interpretive Summary: Necrotic enteritis is a intestinal disease of poultry and its incidence is increasing due to the withdrawl of certain growth promoting drugs. There is very little information concerning the host-pathogen interactions leading to necrotic enteritis. In this report, ARS scientists collaborated with scientists from Schering Plough Animal health and University of Delaware to develop a co-infection model system to reproduce necrotic enteritis. Using this coinfection model using coccidia and clostridium bacteria, host factors involved in local inflammatory immune response was investigated. The results indicate that a pre-exposure of chicken to coccidiosis enhance disease susceptibility to necrotic enteritis and various inflammatory cytokines are produced during necrotic enteritis. Understanding immunological basis of these interactions in necrotic enteritis disease model will lead to new strategy that will reduce economic loss due to these pathogens.
Technical Abstract: We have investigated various aspects of host immune responses using a disease model for necrotic enteritis (NE) in which the severity of lesions produced by Clostridium perfringens was increased, and the growth performance of broiler chickens was decreased by prior infection with Eimeria maxima. Quantitative RT-PCR was used to assess molecular changes in chick intestines that were associated with NE development. During NE, local macrophage activation was repressed as evidenced by reduced expression of iNOS mRNA transcripts. Changes in expression of 17 different immune-related genes show the complexity of the host-pathogen interaction that leads to NE.